pituitrin and Dehydration

In the pregnant patient, hypotonic polyuria in the setting of elevated serum osmolality and polydipsia should narrow the differential to causes related to diabetes insipidus (DI). Gestational DI, also called transient DI of pregnancy, is a distinct entity, unique from central DI or nephrogenic DI which may both become exacerbated during pregnancy. These three different processes relate to vasopressin, where increased metabolism, decreased production or altered renal sensitivity to this neuropeptide should be considered. Gestational DI involves progressively rising levels of placental vasopressinase throughout pregnancy, resulting in decreased endogenous vasopressin and resulting hypotonic polyuria worsening through the pregnancy. Gestational DI should be distinguished from central and nephrogenic DI that may be seen during pregnancy through use of clinical history, urine and serum osmolality measurements, response to desmopressin and potentially, the newer, emerging copeptin measurement. This review focuses on a brief overview of osmoregulatory and vasopressin physiology in pregnancy and how this relates to the clinical presentation, pathophysiology, diagnosis and management of gestational DI, with comparisons to the other forms of DI during pregnancy. Differentiating the subtypes of DI during pregnancy is critical in order to provide optimal management of DI in pregnancy and avoid dehydration and hypernatremia in this vulnerable population.

Topics: Dehydration; Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diabetes Insipidus, Neurogenic; Diagnosis, Differential; Female; Humans; Hypernatremia; Neurophysins; Osmoregulation; Polydipsia; Polyuria; Pregnancy; Pregnancy Complications; Protein Precursors; Vasopressins; Water-Electrolyte Balance

For an endocrinologist, nephrogenic diabetes insipidus (NDI) is an end-organ disease, that is the antidiuretic hormone, arginine-vasopressin (AVP) is normally produced but not recognized by the kidney with an inability to concentrate urine despite elevated plasma concentrations of AVP. Polyuria with hyposthenuria and polydipsia are the cardinal clinical manifestations of the disease. For a geneticist, hereditary NDI is a rare disease with a prevalence of five per million males secondary to loss of function of the vasopressin V2 receptor, an X-linked gene, or loss of function of the water channel AQP2. These are small genes, easily sequenced, with a number of both recurrent and private mutations described as disease causing. Other inherited disorders with mild, moderate or severe inability to concentrate urine include Bartter's syndrome and cystinosis. MAGED2 mutations are responsible for a transient form of Bartter's syndrome with severe polyhydramnios. The purpose of this review is to describe classical phenotype findings that will help physicians to identify early, before dehydration episodes with hypernatremia, patients with familial NDI. A number of patients are still diagnosed late with repeated dehydration episodes and large dilations of the urinary tract leading to a flow obstructive nephropathy with progressive deterioration of glomerular function. Families with ancestral X-linked AVPR2 mutations could be reconstructed and all female heterozygote patients identified with subsequent perinatal genetic testing to recognize affected males within 2 weeks of birth. Prevention of dehydration episodes is of critical importance in early life and beyond and decreasing solute intake will diminish total urine output.

Topics: Dehydration; Diabetes Insipidus, Nephrogenic; Female; Genetic Carrier Screening; Genetic Diseases, X-Linked; Genetic Testing; Humans; Hypernatremia; Infant, Newborn; Kidney Glomerulus; Male; Mutation; Neurophysins; Osmolar Concentration; Pregnancy; Prenatal Diagnosis; Protein Precursors; Receptors, Vasopressin; Vasopressins

Suboptimal fluid intake may require enhanced release of antidiuretic hormone (ADH) or vasopressin for the maintenance of adequate hydration. Enhanced copeptin levels (reflecting enhanced vasopressin levels) in 25% of the common population are associated with enhanced risk of metabolic syndrome with abdominal obesity, type 2 diabetes, hypertension, coronary artery disease, heart failure, vascular dementia, cognitive impairment, microalbuminuria, chronic kidney disease, inflammatory bowel disease, cancer, and premature mortality. Vasopressin stimulates the release of glucocorticoids which in turn up-regulate the serum- and glucocorticoid-inducible kinase 1 (SGK1). Moreover, dehydration upregulates the transcription factor NFAT5, which in turn stimulates SGK1 expression. SGK1 is activated by insulin, growth factors and oxidative stress via phosphatidylinositide-3-kinase, 3-phosphoinositide-dependent kinase PDK1 and mTOR. SGK1 is a powerful stimulator of Na+/K+-ATPase, carriers (e.g. the Na+,K+,2Cl- cotransporter NKCC, the NaCl cotransporter NCC, the Na+/H+ exchanger NHE3, and the Na+ coupled glucose transporter SGLT1), and ion channels (e.g. the epithelial Na+ channel ENaC, the Ca2+ release activated Ca2+ channel Orai1 with its stimulator STIM1, and diverse K+ channels). SGK1 further participates in the regulation of the transcription factors nuclear factor kappa-B NFκB, p53, cAMP responsive element binding protein (CREB), activator protein-1, and forkhead transcription factor FKHR-L1 (FOXO3a). Enhanced SGK1 activity fosters the development of hypertension, obesity, diabetes, thrombosis, stroke, inflammation including inflammatory bowel disease and autoimmune disease, cardiac fibrosis, proteinuria, renal failure as well as tumor growth. The present brief review makes the case that suboptimal fluid intake in the common population may enhance vasopressin and glucocorticoid levels thus up-regulating SGK1 expression and favouring the development of SGK1 related pathologies.

Topics: Dehydration; Disease Susceptibility; Glucocorticoids; Humans; Immediate-Early Proteins; Organism Hydration Status; Protein Serine-Threonine Kinases; Up-Regulation; Vasopressins

Orthostatic hypotension (OH) is defined as a decrease in systolic blood pressure of 20 mmHg, or a decrease in diastolic blood pressure of 10 mmHg within three minutes of standing. It results from an inadequate response to postural changes in blood pressure. Common symptoms include dizziness, light-headedness, blurred vision, weakness, fatigue, nausea, palpitations, sweating, head and neck ache, slow cognitive performance and transient loss of conscientiousness. OH is a common problem among elderly patients and its aetiology is diverse, including autonomic nervous system dysfunction, cardiac problems, medication side effects, ageing changes or transitory deregulation of blood volume. The instrumental diagnosis can be easily accomplished by the tilt-table test, with continuous monitoring of blood pressure and cardiac parameters. It is a non-invasive technique and needs minimal collaboration from the patient. In our experience, when reviewing 327 patients, aged over 40 years and examined because of clinical suspicion of OH, the prevalence thereof was 51% whereas if focused in subjects older than 70, OH was proven in 90% of the cases. The older the patients, the more frequently they presented general deterioration, neurological or cardiac problems as well as pharmacological side effects. Ruling out neurological or cardiac malfunction can drastically improve the prognosis with possible reversibility of symptoms. Some nonpharmacological and pharmacological approaches to improve management of OH and life quality are described for guidance.

Topics: Adult; Age of Onset; Aged; Aged, 80 and over; Autonomic Nervous System Diseases; Cardiovascular Diseases; Central Nervous System Stimulants; Dehydration; Diagnostic Techniques, Neurological; Fludrocortisone; Fluid Therapy; Humans; Hypotension, Orthostatic; Metabolic Diseases; Middle Aged; Stockings, Compression; Sympathomimetics; Vasopressins

Critically ill patients often report distressful episodes of severe thirst, but the complex biochemical, neurohormonal mechanisms that regulate this primal sensation still elude clinicians. The most potent stimuli for thirst are subtle increases in plasma osmolality. These minute changes in osmolality stimulate central osmoreceptors to release vasopressin (also known as antidiuretic hormone). Vasopressin in turn acts on the kidneys to promote the reabsorption of water to correct the increased osmolality. If this compensatory mechanism fails to decrease osmolality, then thirst is triggered to motivate drinking. In contrast, thirst induced by marked volume loss, or hypovolemic thirst, is subject to the tight osmoregulation of the renin-angiotensin aldosterone system and accompanying adrenergic agonists. Understanding the essential role that thirst plays in salt and water regulation can provide clinicians with a better appreciation for the complex physiology that underlies this intense sensation.

Topics: Adrenergic Agonists; Critical Illness; Dehydration; Humans; Hypovolemia; Osmolar Concentration; Perception; Renin-Angiotensin System; Thirst; Vasopressins

Dehydration (body water deficit) is a physiologic state that can have profound implications for human health and performance. Unfortunately, dehydration can be difficult to assess, and there is no single, universal gold standard for decision making. In this article, we review the physiologic basis for understanding quantitative dehydration assessment. We highlight how phenomenologic interpretations of dehydration depend critically on the type (dehydration compared with volume depletion) and magnitude (moderate compared with severe) of dehydration, which in turn influence the osmotic (plasma osmolality) and blood volume-dependent compensatory thresholds for antidiuretic and thirst responses. In particular, we review new findings regarding the biological variation in osmotic responses to dehydration and discuss how this variation can help provide a quantitative and clinically relevant link between the physiology and phenomenology of dehydration. Practical measures with empirical thresholds are provided as a starting point for improving the practice of dehydration assessment.

Topics: Blood Volume; Body Water; Dehydration; Humans; Neurophysins; Osmolar Concentration; Protein Precursors; Thirst; Vasopressins; Water-Electrolyte Balance

Moderate dehydration impairs concentration and co-ordination, whereas severe dehydration can cause seizures, brain damage or death. To slow the progression of dehydration until body fluids can be replenished by drinking, the increased body fluid osmolality associated with dehydration increases vasopressin (antidiuretic hormone) secretion from the posterior pituitary gland. Increased vasopressin secretion reduces water loss in the urine by promoting water reabsorption in the collecting ducts of the kidney. Vasopressin secretion is largely determined by action potential discharge in vasopressin neurones, and depends on both the rate and pattern of discharge. Vasopressin neurone activity depends on intrinsic and extrinsic mechanisms. We review recent advances in our understanding of the physiological regulation of vasopressin neurone activity patterning and the mechanisms by which this is altered to cope with the increased secretory demands of dehydration.

Topics: Action Potentials; Animals; Dehydration; Humans; Neuronal Plasticity; Neurons; Receptors, Opioid, kappa; Vasopressins

Topics: Aquaporin 2; Body Water; Dehydration; Diabetes Insipidus; Edema; Humans; Inappropriate ADH Syndrome; Kidney Concentrating Ability; Mutation; Osmolar Concentration; Sodium; Vasopressins

A thorough presentation of the influence of thyroliberin (TRH) on vasopressin and oxytocin release from the hypothalamo-neurohypophysial system is presented. Thyroliberin affects in different ways both neurohormone secretion in females during lactation according to the water-electrolyte metabolism in the course of the circadian rhythm of vasopressin and oxytocin release as well as during in vitro incubation of isolated neurointermediate lobe or hypothalamo-neurohypohysial explants. The results showed that: TRH acts as a stimulator of oxytocin release into the blood by equilibrated water-electrolyte metabolism, TRH acts in the central nervous system as an inhibitory neuromodulator of vasopressin and oxytocin release from the hypothalamo-neurohypophysial system under in vitro conditions, by osmotic stimulation, as well as in females during lactation, TRH inhibits AVP release in acute bleeding-provoked hypovolemia and alters the circadian rhythm of vasopressin and oxytocin release. It is assumed that this neuropeptide can interact with the mechanisms engaged in vasopressin and oxytocin release and can disturb these mechanisms, especially under conditions of augmented demand of the organism for these neurohormones.

Topics: Animals; Dehydration; Disease Models, Animal; Dogs; Female; Humans; Hypothalamo-Hypophyseal System; Lactation; Male; Oxytocin; Pituitary-Adrenal System; Pregnancy; Rats; Thyrotropin-Releasing Hormone; Thyroxine; Vasopressins; Water; Water Deprivation

Topics: Aldosterone; Atrial Natriuretic Factor; Body Water; Dehydration; Fluid Therapy; Humans; Oliguria; Osmotic Pressure; Renin; Sodium; Vasopressins

Topics: Dehydration; Fluid Therapy; Glucose; Humans; Hyponatremia; Infections; Meningitis; Pediatrics; Sodium Chloride; Vasopressins

Water balance depends essentially on fluid intake and urine excretion. Mild dehydration and the consequent hypertonicity of the extracellular fluid induce an increase in vasopressin secretion, thus stimulating urine concentrating processes and the feeling of thirst. The osmotic threshold for the release of vasopressin is lower than that for thirst and also shows appreciable individual variation. Sustained high levels of vasopressin and low hydration induce morphological and functional changes in the kidney. However, they could also be risk factors in several renal disorders, such as chronic renal failure, diabetic nephropathy and salt-sensitive hypertension.

Topics: Animals; Dehydration; Humans; Kidney; Kidney Concentrating Ability; Kidney Diseases; Rats; Thirst; Urination; Vasopressins; Water-Electrolyte Balance

Angiotensinogen, the precursor molecule of the peptides angiotensin I, II, and III, is synthesized in the brain and the liver. Evidence is reviewed that angiotensin II, and possibly angiotensin III, that are generated within the brain act within neural circuits of the central nervous system to regulate body fluid balance. Immunohistochemical studies in the rat brain have provided evidence of angiotensin-containing neurons, especially in the hypothalamic paraventricular nucleus, subfornical organ, periventricular region, and nucleus of the solitary tract, as well as in extensive angiotensin-containing fiber pathways. Angiotensin immunoreactivity is observed by electron microscope in synaptic vesicles in several brain regions, the most prominent of these being the central nucleus of the amygdala. Neurons in many parts of the brain (lamina terminalis, paraventricular and parabrachial nuclei, ventrolateral medulla, and nucleus of the solitary tract) known to be involved in the regulation of body fluid homeostasis exhibit angiotensin receptors of the AT(1) subtype. Pharmacological studies in several species show that intracerebroventricular administration of AT(1) receptor antagonist drugs inhibit homeostatic responses to the central administration of hypertonic saline, intravenous infusion of the hormone relaxin, or thermal dehydration. Responses affected by centrally administered AT(1) antagonists are water drinking, vasopressin secretion, natriuresis, increased arterial pressure, reduced renal renin release, salt hunger, and thermoregulatory adjustments. We conclude that angiotensinergic neural pathways in the brain probably have an important homeostatic function, especially in regard to osmoregulation and thermoregulation, and the maintenance of arterial pressure.

Topics: Angiotensin II; Angiotensin III; Animals; Blood Pressure; Body Temperature Regulation; Brain; Dehydration; Drinking Behavior; Homeostasis; Humans; Kidney; Neurons; Receptors, Angiotensin; Renin; Synaptic Vesicles; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Cell Membrane Permeability; Dehydration; Extracellular Space; Kidney Medulla; Kidney Tubules, Collecting; Osmotic Pressure; Rats; Vasopressins; Water

Topics: Animals; Dehydration; Glomerular Filtration Rate; Homozygote; Humans; Kidney Concentrating Ability; Osmolar Concentration; Oxytocin; Rats; Rats, Brattleboro; Vasopressins

Topics: Blood Volume; Child; Craniocerebral Trauma; Deamino Arginine Vasopressin; Dehydration; Diabetes Mellitus, Type 1; Diuresis; Female; Humans; Kinetics; Male; Models, Biological; Neurophysins; Osmolar Concentration; Oxytocin; Pituitary Gland, Posterior; Postoperative Complications; Pregnancy; Pregnancy in Diabetics; Thirst; Urine; Vasopressins

Topics: Animals; Dehydration; Guinea Pigs; Oxytocin; Paraventricular Hypothalamic Nucleus; Pituitary Gland, Posterior; Rats; Receptors, Adrenergic; Receptors, Cholinergic; Supraoptic Nucleus; Synaptic Transmission; Vasopressins; Water-Electrolyte Balance

Clinical disorders of water regulation are relatively common and occur with severity ranging from profound and easily recognizable disturbance of body water balance to mild and often clinically inapparent. The development of sensitive and specific radioimmunoassay procedures capable of quantitating the level of AVP in plasma and urine has allowed elucidation of the pathophysiology of many of the disorders whether due to deficiency of ADH secretion and action or to excessive or persistent hormone release. In turn, the understanding of the factors regulating ADH release and action has led to establishment and validation of a variety of procedures that by indirect means allow estimation of extent of hormone action. These procedures based on physiologic influences that stimulate or inhibit ADH release or action are simple, readily available, and relatively inexpensive, and are capable of making an accurate diagnosis of a water-losing or water-retaining disorder. Properly performed and interpreted, such tests as water deprivation, saline infusion, comparison of urine and serum osmolality, and water loading can obviate the need for AVP immunoassays in evaluating most clinical disorders of water regulation. The immunoassay of AVP, although a valuable tool for the study of normal and pathologic physiology of ADH, is rarely necessary to firmly establish a clinical diagnosis and may itself be the source of misleading conclusions if its limitations are not fully appreciated.

Topics: Arginine Vasopressin; Body Water; Dehydration; Endocrine System Diseases; Humans; Osmolar Concentration; Radioimmunoassay; Vasopressins

Topics: Adrenal Glands; Animals; Dehydration; Diabetes Insipidus; Diet; Dose-Response Relationship, Drug; Glomerular Filtration Rate; Hemodynamics; Kidney; Osmolar Concentration; Potassium; Prostaglandins; Rats; Rats, Brattleboro; Rats, Mutant Strains; Sodium; Vasopressins; Water-Electrolyte Balance

Water balance is tightly regulated within a tolerance of less than 1 percent by a physiologic control system located in the hypothalamus. Body water homeostasis is achieved by balancing renal and nonrenal water losses with appropriate water intake. The major stimulus to thirst is increased osmolality of body fluids as perceived by osmoreceptors in the anteroventral hypothalamus. Hypovolemia also has an important effect on thirst which is mediated by arterial baroreceptors and by the renin-angiotensin system. Renal water loss is determined by the circulating level of the antidiuretic hormone, arginine vasopressin (AVP). AVP is synthesized in specialized neurosecretory cells located in the supraoptic and paraventricular nuclei in the hypothalamus and is transported in neurosecretory granules down elongated axons to the posterior pituitary. Depolarization of the neurosecretory neurons results in the exocytosis of the granules and the release of AVP and its carrier protein (neurophysin) into the circulation. AVP is secreted in response to a wide variety of stimuli. Change in body fluid osmolality is the most potent factor affecting AVP secretion, but hypovolemia, the renin-angiotensin system, hypoxia, hypercapnia, hyperthermia and pain also have important effects. Many drugs have been shown to stimulate the release of AVP as well. Small changes in plasma AVP concentration of from 0.5 to 4 muU per ml have major effects on urine osmolality and renal water handling.

Topics: Adolescent; Adult; Aged; Animals; Arginine Vasopressin; Blood Volume; Body Fluids; Body Water; Child; Child, Preschool; Dehydration; Diabetes Insipidus; Dogs; Female; Homeostasis; Humans; Hyperaldosteronism; Hypothalamus; Infant; Infant, Newborn; Kidney; Male; Middle Aged; Osmosis; Rats; Sheep; Thirst; Vasopressins; Water-Electrolyte Balance

Topics: Action Potentials; Afferent Pathways; Aldosterone; Angiotensin II; Animals; Autonomic Nervous System; Blood Glucose; Conditioning, Classical; Dehydration; Diuresis; Drinking; Efferent Pathways; Energy Metabolism; Female; Glucagon; Humans; Infusions, Parenteral; Insulin; Insulin Secretion; Male; Mouth; Pancreas; Rats; Stomach; Sweating; Taste Buds; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Animals; Body Fluid Compartments; Body Fluids; Body Water; Brain; Dehydration; Diabetes Insipidus; Extracellular Space; Glucose; Homeostasis; Humans; Hyperglycemia; Infant, Newborn; Intracellular Fluid; Male; Osmolar Concentration; Plasma; Sodium; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Diagnostic approaches evolve steadily. Selective renal arteriography and determination of renal vein renins have replaced differential clearances and translumbar aortography. The hydrated intravenous pyelogram remains helpful in assessing physiologic significance and complements both aortography and renin determinations. Except for young patients, medical treatment rather than surgical management usually is preferred.

Topics: Adult; Creatinine; Dehydration; Female; Humans; Hydrogen-Ion Concentration; Hypertension, Renal; Kidney Function Tests; Middle Aged; Renal Artery Obstruction; Renin; Saline Solution, Hypertonic; Sodium; Sodium Chloride; Urography; Vasopressins; Water-Electrolyte Balance

Topics: Adenylyl Cyclases; Adrenal Glands; Adult; Animals; Body Water; Chlorpropamide; Dehydration; Diabetes Insipidus; Genes; Growth Hormone; Heterozygote; Humans; Hyponatremia; Hypothalamus; Oxytocin; Pituitary Gland; Pituitary Gland, Posterior; Rats; Sodium; Vasopressins

Topics: Adult; Biological Assay; Blood; Blood Pressure; Blood Volume; Dehydration; Diabetes Insipidus; Humans; Kidney Concentrating Ability; Osmolar Concentration; Polyuria; Posture; Radioimmunoassay; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Albumins; Animals; Biological Transport, Active; Calcium; Chlorides; Dehydration; Diuresis; Extracellular Space; Hydrogen-Ion Concentration; Inulin; Kidney Tubules; Kidney Tubules, Distal; Kidney Tubules, Proximal; Magnesium; Nephrons; Phosphorus; Potassium; Radioisotopes; Sodium; Sodium Chloride; Sodium Isotopes; Tritium; Vasopressins

Topics: Acute Kidney Injury; Animals; Blood; Cardiac Glycosides; Dehydration; Diuretics; Glomerular Filtration Rate; Heart Failure; Hyponatremia; Kidney Failure, Chronic; Liver Cirrhosis; Mineralocorticoid Receptor Antagonists; Nephrotic Syndrome; Sodium; Syndrome; Vasopressins; Water

Topics: Amphetamine; Angiotensin II; Barbiturates; Brain Damage, Chronic; Cardiac Glycosides; Computers; Dehydration; Diuretics; Drinking; Drinking Behavior; Eating; Electric Stimulation; Electrolytes; Endocrine Glands; Hot Temperature; Humans; Hypothyroidism; Insulin; Kidney; Parasympatholytics; Parasympathomimetics; Renin; Serotonin; Thirst; Time Factors; Vasopressins

Topics: Body Weight; Dehydration; Diabetes Insipidus; Diagnosis, Differential; Humans; Hypertonic Solutions; Injections, Intramuscular; Injections, Intravenous; Isotonic Solutions; Nicotine; Polyuria; Smoking; Sodium Chloride; Sulfonylurea Compounds; Thirst; Vasopressins

Topics: Angiography; Biological Transport, Active; Contrast Media; Dehydration; Diuresis; Furosemide; Glomerular Filtration Rate; Humans; Hypertension; Kidney; Kidney Calculi; Kidney Concentrating Ability; Kidney Failure, Chronic; Kidney Tubules; Male; Metaraminol; Prostatic Diseases; Renal Artery Obstruction; Sodium; Urinary Calculi; Urography; Vasopressins

Topics: Accidents, Traffic; Acidosis; Acute Kidney Injury; Adult; Aged; Alkalosis; Aortic Diseases; Aortic Rupture; Body Composition; Calorimetry; Cholecystectomy; Convalescence; Craniocerebral Trauma; Dehydration; Duodenal Ulcer; Endocrine Glands; Female; Homeostasis; Humans; Iliac Artery; Infusions, Parenteral; Kidney; Lung Neoplasms; Male; Metabolism; Middle Aged; Natriuresis; Pancreatitis; Peptic Ulcer Perforation; Postoperative Care; Postoperative Complications; Thoracic Injuries; Thrombosis; Vasopressins; Water-Electrolyte Balance

Topics: Adolescent; Adult; Aged; Animals; Arginine; Child; Dehydration; Diabetes Insipidus; Female; Humans; Hyperaldosteronism; Hypertonic Solutions; Hypocalcemia; Kidney Failure, Chronic; Kidney Transplantation; Kidney Tubules; Male; Middle Aged; Nicotine; Osmolar Concentration; Polyuria; Sex Factors; Sodium Chloride; Thirst; Time Factors; Urine; Urologic Diseases; Vasopressins; Water-Electrolyte Balance

Topics: Dehydration; Glucose; Humans; Hypertonic Solutions; Nicotine; Osmotic Pressure; Oxytocin; Pituitary Function Tests; Sodium; Vasopressins

Water intake occurs following a period of high-intensity intermittent exercise (HIIE) due to sensations of thirst yet this does not always appear to be caused by body water losses. Thu.s, the aim was to assess voluntary water intake following HIIE. Ten healthy males (22 ± 2 y, 75.6 ± 6.9 kg, VO2(peak) 57.3 ± 11.4 m · kg(-1) · min(-1); mean ± SD) completed two trials (7-14 d apart). Subjects sat for 30 min then completed an exercise period involving 2 min of rest followed by 1 min at 100% VO2(peak repeated for 60 min (HIIE) or 60 min continuously at 33% VO2(peak) (LO). Subjects then sat for 60 min and were allowed ad libitum water intake. Body )mass was measured at start and end of trials. Serum osmolality, blood lactate, and sodium concentrations, sensations of thirst and mouth dryness were measured at baseline, postexercise and after 5, 15, 30, and 60 min of recovery. Vasopressin concentration was measured at baseline, postexercise, 5 min, and 30 min. Body mass loss over the whole trial was similar (HIIE: 0.77 ± 0.50; LO: 0.85 ± 0.55%; p = .124). Sweat lost during exercise (0.78 ± 0.22 vs. 0.66 ± 0.26 L) and voluntary water intake during recovery (0.416 ± 0.299 vs. 0.294 ± 0.295 L; p < .05) were greater in HIIE. Serum osmolality (297 ± 3 vs. 288 ± 4 mOsmol · kg(-1)), blood lactate (8.5 ± 2.7 vs. 0.7 ± 0.4 mmol · L(-1)), serum sodium (146 ± 1 vs. 143 ± 1 mmol · L(-1)) and vasopressin (9.91 ± 3.36 vs. 4.43 ± 0.86 pg · ml(-1)) concentrations were higher after HIIE (p < .05) and thirst (84 ± 7 vs. 60 ± 21) and mouth dryness (87 ± 7 vs. 64 ± 23) also tended to be higher (p = .060). Greater voluntary water intake after HIIE was mainly caused by increased sweat loss and the consequences of increased serum osmolality mainly resulting from higher blood lactate concentrations.

Topics: Adult; Body Water; Dehydration; Drinking; Drinking Water; Exercise; Heart Rate; Humans; Lactic Acid; Male; Mouth; Osmolar Concentration; Physical Exertion; Rest; Sodium; Sweat; Sweating; Thirst; Vasopressins; Water-Electrolyte Balance; Weight Loss; Young Adult

We examined whether carbohydrate in beverages accelerated fluid retention during recovery from thermal and exercise-induced dehydration and whether it was caused in part by an enhanced renal Na+ reabsorption rate due to insulin secretion. After dehydrating by ∼2.3% body weight by exercise in a hot environment, seven young men underwent high-carbohydrate, low-carbohydrate, or control rehydration trials by drinking one of three beverages with 3.4 g glucose + 3.1 g fructose, 1.7 g glucose + 1.6 g fructose, or 0.0 g glucose + 0.0 g fructose per deciliter, respectively, in a common composition of electrolyte solution: 21 meq/l [Na+], 5 meq/l [K+], 16.5 meq/l [Cl-], 10 meq/l [citrate(-3)]. They drank the same amount of beverage as total body weight loss within 30 min. During the 60 min before the start of drinking and the following 180 min, we measured plasma volume (PV), plasma glucose ([Glc]p), serum insulin ([Ins]s), plasma Na+ concentrations, and the renal clearances of inulin, lithium, and Na+ with plasma vasopressin ([AVP]p) and aldosterone concentrations ([Ald]p) every 30 min. After dehydration, PV decreased by ∼5% and plasma osmolality increased by ∼6 mosmol/kg H2O in all trials with no significant differences among them. We found in the high-carbohydrate trial that 1) PV increased faster than in the control trial and remained at the higher level than other trials for the last 60 min (P < 0.05); 2) accumulated urine volume was smallest after 90 min (P < 0.05); 3) the renal Na+ reabsorption rate was greatest for the first 120 min (P < 0.05); 4) during which period [AVP]p and [Ald](p) were not significantly different from other trials (both, P > 0.9); and 5) [Glc](p) and [Ins]s were highest from 45 to 105 min (P < 0.05) during rehydration. Thus carbohydrate in beverages enhances renal Na+ reabsorption, and insulin is possibly involved in this enhancement.

Topics: Adult; Aldosterone; Analysis of Variance; Beverages; Bicycling; Biomarkers; Blood Glucose; Dehydration; Dietary Carbohydrates; Environment; Exercise; Exercise Test; Fructose; Glomerular Filtration Rate; Glucose; Hot Temperature; Humans; Insulin; Japan; Kidney Tubules; Least-Squares Analysis; Male; Natriuresis; Neurophysins; Osmolar Concentration; Plasma Volume; Protein Precursors; Recovery of Function; Rehydration Solutions; Sodium; Time Factors; Urodynamics; Vasopressins; Water-Electrolyte Balance; Young Adult

Evidence of the effect of dehydration on physiological responses to hypoxia is limited. The purpose of this study was to determine the effect of hypohydration severity on physiological, renal hormonal and psychological responses to acute hypoxia. Eight males completed intermittent walking tests under normobaric hypoxic conditions (FI O(2) = 0.13) after completing four separate hypohydration protocols, causing change in body mass of approximately 0% (EU), -1% (H1), -2% (H2) and -3% (H3). Physiological and psychological markers were monitored throughout the 125 min test. Fluid controlling hormones were measured pre and post exposure. Heart rate, core temperature, peripheral arterial oxygen saturation (SpO(2)), minute ventilation and urine osmolality were found to be significantly different between hydration conditions and correlated with Lake Louise Questionnaire score (LLQ) (P < 0.05). LLQ score increased with hypohydration severity above H2 (EU 1.3 +/- 1; H1 1.2 +/- 1; H2 2.7 +/- 2; H3 3.9 +/- 2) (P < 0.001). Antidiuretic hormone and aldosterone increased over the test, but were not different between hydration conditions (P < 0.05). Atrial natriuretic peptide showed no change over time, or with conditions. Therefore, renal hormones are not influenced by hypohydration severity during moderate intensity hypoxic exercise. Hypohydration less than -2% induces greater physiological strain during hypoxic exercise and may cause rise in symptoms such as, fatigue, headache, nausea and lightheadedness.

Topics: Adaptation, Physiological; Adaptation, Psychological; Adult; Aldosterone; Algorithms; Body Weight; Dehydration; Exercise; Heart Rate; Hormones; Humans; Kidney; Male; Oxygen; Vasopressins; Young Adult

During exercise-heat stress, ad libitum drinking frequently fails to match sweat output, resulting in deleterious changes in hormonal, circulatory, thermoregulatory, and psychological status. This condition, known as voluntary dehydration, is largely based on perceived thirst. To examine the role of preexercise dehydration on thirst and drinking during exercise-heat stress, 10 healthy men (21 +/- 1 yr, 57 +/- 1 ml x kg(-1) x min(-1) maximal aerobic power) performed four randomized walking trials (90 min, 5.6 km/h, 5% grade) in the heat (33 degrees C, 56% relative humidity). Trials differed in preexercise hydration status [euhydrated (Eu) or hypohydrated to -3.8 +/- 0.2% baseline body weight (Hy)] and water intake during exercise [no water (NW) or water ad libitum (W)]. Blood samples taken preexercise and immediately postexercise were analyzed for hematocrit, hemoglobin, serum aldosterone, plasma osmolality (P(osm)), plasma vasopressin (P(AVP)), and plasma renin activity (PRA). Thirst was evaluated at similar times using a subjective nine-point scale. Subjects were thirstier before (6.65 +/- 0.65) and drank more during Hy+W (1.65 +/- 0.18 liters) than Eu+W (1.59 +/- 0.41 and 0.31 +/- 0.11 liters, respectively). Postexercise measures of P(osm) and P(AVP) were significantly greater during Hy+NW and plasma volume lower [Hy+NW = -5.5 +/- 1.4% vs. Hy+W = +1.0 +/- 2.5% (P = 0.059), Eu+NW = -0.7 +/- 0.6% (P < 0.05), Eu+W = +0.5 +/- 1.6% (P < 0.05)] than all other trials. Except for thirst and drinking, however, no Hy+W values differed from Eu+NW or Eu+W values. In conclusion, dehydration preceding low-intensity exercise in the heat magnifies thirst-driven drinking during exercise-heat stress. Such changes result in similar fluid regulatory hormonal responses and comparable modifications in plasma volume regardless of preexercise hydration state.

Topics: Adult; Aldosterone; Body Mass Index; Body Weight; Dehydration; Drinking; Exercise; Hematocrit; Hemodynamics; Hemoglobins; Hormones; Hot Temperature; Humans; Male; Osmolar Concentration; Renin; Thirst; Vasopressins; Walking

In rats, the hypothalamic neurotransmitter histamine participates in regulation of vasopressin secretion and seems to be of physiological importance, because blockade of the histaminergic system reduces dehydration-induced vasopressin secretion. We investigated whether histamine is also involved in regulation of vasopressin secretion during dehydration in humans. We found that 40 h of dehydration gradually increased plasma osmolality by 10 mosmol/kg and induced a fourfold increase in vasopressin levels. Pretreatment with the H(2)-receptor antagonists cimetidine or ranitidine significantly reduced the dehydration-induced increase in vasopressin levels approximately 40% after 34 and 37 h of dehydration, whereas this was not the case with the H(1)-receptor antagonist mepyramine. Dehydration reduced aldosterone secretion by approximately 50%. This effect of dehydration was reduced by both H(1)- and H(2)-receptor blockade after 16 and/or 34 h of dehydration. We conclude that vasopressin secretion in response to dehydration in humans is under the regulatory influence of histamine and that the effect seems to be mediated via H(2)-receptors. In addition, the regulation of aldosterone secretion during dehydration also seems to involve the histaminergic system via H(1) and H(2) receptors.

Topics: Adult; Aldosterone; Cimetidine; Cross-Over Studies; Dehydration; Double-Blind Method; Histamine H1 Antagonists; Histamine H2 Antagonists; Humans; Male; Osmolar Concentration; Placebos; Pyrilamine; Ranitidine; Receptors, Histamine H1; Receptors, Histamine H2; Vasopressins; Water-Electrolyte Balance

On two separate occasions six trained subjects (peak oxygen consumption [VO2peak] 4.41/min) rode for 60 min at 70% of VO2peak and then to exhaustion at 90% of VO2peak to determine the effects of mild dehydration on high-intensity cycling performance time in the heat (32 degrees C, 60% relative humidity, wind speed 3 km/h). In one trial (F) subjects ingested a 400 ml bolus of 20 mmol/l NaCl immediately before, and then as repetitive 120 ml feedings every 10 min during the first 50 min of exercise. In the other trial they did not ingest fluid (NF) either before or during exercise. The order of testing was in a counter-balanced random sequence. For the first 60 min of exercise mean (+/- SD) VO2 (2.90 +/- 0.39 vs 2.93 +/- 0.38 l/min) and respiratory exchange ratio (RER; 0.95 +/- 0.03 vs 0.94 +/- 0.04) values were similar between F and NF trials. However, weight loss was significantly reduced during F compared to NF (0.16 +/- 0.39 vs 1.30 +/- 0.22 kg; p < 0.005) and high-intensity cycling time to exhaustion was significantly increased (9.8 +/- 3.9 vs 6.8 +/- 3.0 min; p < 0.005). Increased cycling times to exhaustion in the F trial were not associated with any measurable differences in heart rate (HR), body temperature, respiratory gas exchange, leg muscle power over 5 sec, or the degree to which fluid ingestion reduced the level of dehydration within the group. Only the ratings of perceived exertion (RPE) and plasma anti diuretic hormone (ADH) concentrations were significantly increased in the NF trial compared to the F trial.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Bicycling; Body Temperature; Dehydration; Fluid Therapy; Heart Rate; Hot Temperature; Humans; Humidity; Male; Muscle Contraction; Oxygen Consumption; Perception; Physical Endurance; Physical Exertion; Psychomotor Performance; Respiration; Sodium Chloride; Time Factors; Vasopressins; Weight Loss; Wind

Topics: Acromegaly; Adult; Arginine; Blood; Clinical Trials as Topic; Cortisone; Dehydration; Dexamethasone; Diethylstilbestrol; Diuresis; Female; Growth Hormone; Humans; Male; Middle Aged; Nicotine; Osmolar Concentration; Pituitary Function Tests; Pituitary Gland, Posterior; Urine; Vasopressins

Topics: Clinical Trials as Topic; Dehydration; Diatrizoate; Humans; Injections, Intravenous; Kidney Tubules; Osmolar Concentration; Urography; Vasopressins; Water-Electrolyte Balance

We examined the effects of rapid restriction of food and fluid intake on the pathways of water homeostasis, the vasopressinergic system (VPS), and the renin-angiotensin-aldosterone system (RAAS), in rats with or without regular exercise.. Sprague Dawley rats were divided into the following groups: no intervention, rapid restriction, regular exercise, and rapid restriction combined with regular exercise. Rats in the exercise group performed climbing exercise for 4 weeks. All rats consumed food ad libitum, and those in the rapid restriction group fasted for the last 3 days with no water on the last 1 day.. Despite no significant differences in body weight among the groups, the kidney weight was decreased when rapid restriction and regular exercise were combined. Rapid restriction reduced the urine volume and increased the urine osmolality, whereas regular exercise did not. Rapid restriction but not regular exercise increased the levels of circulating aldosterone and the renal expression levels of the ion channel SGK-1 compared to those without rapid restriction, indicating the stimulation of RAAS. Conversely, VPS showed no significant response to these interventions. Moreover, rapid restriction combined with regular exercise induced the renal expression levels of proinflammatory cytokines and increased the active forms of apoptotic effector caspase-3 compared with the no intervention group.. Functional significance may differ between VPS and RAAS in water homeostasis in response to rapid restriction. Moreover, the combination of rapid restriction and regular exercise has potentially deleterious effects on the kidney.

Topics: Animals; Dehydration; Fasting; Homeostasis; Kidney Diseases; Male; Models, Animal; Physical Conditioning, Animal; Rats; Rats, Sprague-Dawley; Renin-Angiotensin System; Vasopressins; Water

Vasopressin is elevated in response to heat and dehydration and has been postulated to have a role in the chronic kidney disease of unknown origin being observed in Central America. The aims of this study were to examine whether the vasopressin pathway, as measured by copeptin, is associated with the presence of kidney dysfunction, and to examine whether higher fluid intake is associated with lower circulating copeptin and thereby preserves kidney health among sugarcane workers exposed to hot conditions.. Utilizing a longitudinal study of 105 workers in Guatemala, we examined relationships between hydration indices, plasma copeptin concentrations, and kidney function markers at 3 times during the 6-month harvest. We also examined whether baseline copeptin concentrations increased the odds of developing an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2.. Copeptin concentrations were positively associated with serum creatinine (β 1.41, 95% CI 0.88-2.03) and negatively associated with eGFR (β -1.07, 95% CI -1.43 to -0.70). In addition, as workers improved their hydration (measured by increases in fluid balance), copeptin concentrations were reduced, and this reduction was associated with an improvement in kidney function.. Results suggest that copeptin should be studied as a potential prognostic biomarker.

Topics: Adult; Agricultural Workers' Diseases; Biomarkers; Dehydration; Glycopeptides; Guatemala; Hot Temperature; Humans; Kidney; Kidney Function Tests; Longitudinal Studies; Male; Neurophysins; Occupational Exposure; Prevalence; Prognosis; Prospective Studies; Protein Precursors; Renal Insufficiency, Chronic; Saccharum; Vasopressins

Topics: Brain; Congresses as Topic; Dehydration; Drinking; Humans; Kidney Diseases; Neurophysins; Neurosecretory Systems; Protein Precursors; Urinary Tract Infections; Vasopressins; Water; Water-Electrolyte Balance

The neurohormones arginine-vasopressin (AVP) and oxytocin (OT) synthesised in supraoptic and paraventricular nuclei of neurohypophysis regulate lactation, systemic water homeostasis and nociception. Using transgenic rats expressing AVP and OT tagged with fluorescent proteins we demonstrate that both neurohormones are expressed in sensory neurones both in vitro, in primary cultures, and in situ, in the intact ganglia; this expression was further confirmed with immunocytochemistry. Both neurohormones were expressed in nociceptive neurones immunopositive to transient receptor potential vannilloid 1 (TRPV1) channel antibodies. The AVP and OT-expressing DRG neurones responded to AVP, OT, 50 mM K

Topics: Animals; Dehydration; Exocytosis; Female; Fluorescence; Ganglia, Spinal; Lactation; Male; Nociception; Oxytocin; Pituitary Gland, Posterior; Rats, Transgenic; Receptors, Oxytocin; Receptors, Vasopressin; Sensory Receptor Cells; Vasopressins

Fructose stimulates vasopressin in humans and can be generated endogenously by activation of the polyol pathway with hyperosmolarity. We hypothesized that fructose metabolism in the hypothalamus might partly control vasopressin responses after acute dehydration. Wild-type and fructokinase-knockout mice were deprived of water for 24 h. The supraoptic nucleus was evaluated for vasopressin and markers of the aldose reductase-fructokinase pathway. The posterior pituitary vasopressin and serum copeptin levels were examined. Hypothalamic explants were evaluated for vasopressin secretion in response to exogenous fructose. Water restriction increased serum and urine osmolality and serum copeptin in both groups of mice, although the increase in copeptin in wild-type mice was larger than that in fructokinase-knockout mice. Water-restricted, wild-type mice showed an increase in vasopressin and aldose reductase mRNA, sorbitol, fructose and uric acid in the supraoptic nucleus. In contrast, fructokinase-knockout mice showed no change in vasopressin or aldose reductase mRNA, and no changes in sorbitol or uric acid, although fructose levels increased. With water restriction, vasopressin in the pituitary of wild-type mice was significantly less than that of fructokinase-knockout mice, indicating that fructokinase-driven vasopressin secretion overrode synthesis. Fructose increased vasopressin release in hypothalamic explants that was not observed in fructokinase-knockout mice. In situ hybridization documented fructokinase mRNA in the supraoptic nucleus, paraventricular nucleus and suprachiasmatic nucleus. Acute dehydration activates the aldose reductase-fructokinase pathway in the hypothalamus and partly drives the vasopressin response. Exogenous fructose increases vasopressin release in hypothalamic explants dependent on fructokinase. Nevertheless, circulating vasopressin is maintained and urinary concentrating is not impaired.. This study increases our understanding of the mechanisms leading to vasopressin release under conditions of water restriction (acute dehydration). Specifically, these studies suggest that the aldose reductase-fructokinase pathways may be involved in vasopressin synthesis in the hypothalamus and secretion by the pituitary in response to acute dehydration. Nevertheless, mice undergoing water restriction remain capable of maintaining sufficient vasopressin (copeptin) levels to allow normal urinary concentration. Further studies of the aldose reductase-fructokinase system in vasopressin regulation appear indicated.

Topics: Analysis of Variance; Animals; Dehydration; Enzyme-Linked Immunosorbent Assay; Fructokinases; Fructose; Gene Expression Regulation; Hot Temperature; Hypothalamus; Mice; Mice, Inbred C57BL; Mice, Knockout; Organ Culture Techniques; RNA, Messenger; Time Factors; Vasopressins; Water Deprivation

The oxytocin (OT) and vasopressin (VP) neurons of the supraoptic nucleus (SON) demonstrate characteristics of "metabolic sensors". They express insulin receptors and glucokinase (GK). They respond to an increase in glucose and insulin with an increase in intracellular [Ca(2+)] and increased OT and VP release that is GK dependent. Although this is consistent with the established role of OT as an anorectic agent, how these molecules function relative to the important role of OT during lactation and whether deficits in this metabolic sensor function contribute to obesity remain to be examined. Thus, we evaluated whether insulin and glucose-induced OT and VP secretion from perifused explants of the hypothalamo-neurohypophyseal system are altered during lactation and by diet-induced obesity (DIO). In explants from female day 8 lactating rats, increasing glucose (Glu, 5 mM) did not alter OT or VP release. However, insulin (Ins; 3 ng/ml) increased OT release, and increasing the glucose concentration in the presence of insulin (Ins+Glu) resulted in a sustained elevation in both OT and VP release that was not prevented by alloxan, a GK inhibitor. Explants from male DIO rats also responded to Ins+Glu with an increase in OT and VP regardless of whether obesity had been induced by feeding a high-fat diet (HFD). The HFD-DIO rats had elevated body weight, plasma Ins, Glu, leptin, and triglycerides. These findings suggest that the role of SON neurons as metabolic sensors is diminished during lactation, but not in this animal model of obesity.

Topics: Alloxan; Animals; Dehydration; Diet, High-Fat; Dietary Fats; Enzyme Inhibitors; Female; Glucokinase; Glucose; In Vitro Techniques; Insulin; Lactation; Neurons; Obesity; Oxytocin; Rats; Rats, Sprague-Dawley; Receptor, Insulin; Supraoptic Nucleus; Vasopressins

The synthesis of arginine vasopressin (AVP) in the supraoptic nucleus (SON) and paraventricular nucleus (PVN) of the hypothalamus is sensitive to increased plasma osmolality and a decreased blood volume, and thus is robustly increased by both dehydration (increased plasma osmolality and decreased blood volume) and salt loading (increased plasma osmolality). Both stimuli result in functional remodelling of the SON and PVN, a process referred to as functional-related plasticity. Such plastic changes in the brain have recently been associated with altered patterns of DNA methylation at CpG (cytosine-phosphate-guanine) residues, a process considered to be important for the regulation of gene transcription. In this regard, the proximal Avp promoter contains a number of CpG sites and is recognised as one of four CpG islands for the Avp gene, suggesting that methylation may be regulating Avp transcription. In the present study, we show that, in an immortalised hypothalamic cell line 4B, the proximal Avp promoter is highly methylated, and treatment of these cells with the DNA methyltransferase inhibitor 5-Aza-2'-deoxycytidine to demethylate DNA dramatically increases basal and stimulated Avp biosynthesis. We report no changes in the expression of DNA methyltransferases, Dnmt1 and Dnmt3a, whereas there is decreased expression of the demethylating enzyme ten-eleven-translocation 2, Tet2, in the SON by dehydration and salt loading. We found higher methylation of the SON Avp promoter in dehydrated but not salt-loaded rats. By analysis of individual CpG sites, we observed hypomethylation, hypermethylation and no change in methylation of specific CpGs in the SON Avp promoter of the dehydrated rat. Using reporter gene assays, we show that mutation of individual CpGs can result in altered Avp promoter activity. We propose that methylation of the SON Avp promoter is necessary to co-ordinate the duel inputs of increased plasma osmolality and decreased blood volume on Avp transcription in the chronically dehydrated rat.

Topics: Animals; Azacitidine; Cell Line; Decitabine; Dehydration; Demethylation; DNA (Cytosine-5-)-Methyltransferase 1; DNA (Cytosine-5-)-Methyltransferases; DNA Methylation; DNA Methyltransferase 3A; Epigenesis, Genetic; Hypothalamus; Male; Mutation; Osmolar Concentration; Promoter Regions, Genetic; Rats; Sodium Chloride; Vasopressins

The magnocellular vasopressin (AVP) and oxytocin (OT) neurones exhibit specific electrophysiological behaviour, synthesise AVP and OT peptides and secrete them into the neurohypophysial system in response to various physiological stimulations. The activity of these neurones is regulated by the very same peptides released either somato-dendritically or when applied to supraoptic nucleus (SON) preparations in vitro. The AVP and OT, secreted somato-dendritically (i.e. in the SON proper) act through specific autoreceptors, induce distinct Ca(2+) signals and regulate cellular events. Here, we demonstrate that about 70% of freshly isolated individual SON neurones from the adult non-transgenic or transgenic rats bearing AVP (AVP-eGFP) or OT (OT-mRFP1) markers, produce distinct spontaneous [Ca(2+)]i oscillations. In the neurones identified (through specific fluorescence), about 80% of AVP neurones and about 60% of OT neurones exhibited these oscillations. Exposure to AVP triggered [Ca(2+)]i oscillations in silent AVP neurones, or modified the oscillatory pattern in spontaneously active cells. Hyper- and hypo-osmotic stimuli (325 or 275 mOsmol/l) respectively intensified or inhibited spontaneous [Ca(2+)]i dynamics. In rats dehydrated for 3 or 5days almost 90% of neurones displayed spontaneous [Ca(2+)]i oscillations. More than 80% of OT-mRFP1 neurones from 3 to 6-day-lactating rats were oscillatory vs. about 44% (OT-mRFP1 neurones) in virgins. Together, these results unveil for the first time that both AVP and OT neurones maintain, via Ca(2+) signals, their remarkable intrinsic in vivo physiological properties in an isolated condition.

Topics: Animals; Calcium; Calcium Signaling; Dehydration; Green Fluorescent Proteins; Male; Neurons; Osmolar Concentration; Oxytocin; Rats, Wistar; Supraoptic Nucleus; Vasopressins

Disorders of water balance are a common feature of clinical practice. An understanding of the physiology and pathophysiology of central vasopressin release and perception of thirst is the key to diagnosis and management of these disorders. Mammals are osmoregulators; they have evolved mechanisms that maintain extracellular fluid osmolality near a stable value, and, in animal studies, osmoregulatory neurons express a truncated delta-N variant of the transient receptor potential vannilloid (TRPV1) channel involved in hypertonicity and thermal perception while systemic hypotonicity might be perceived by TRPV4 channels. Recent cellular and optogenetic animal experiments demonstrate that, in addition to the multifactorial process of excretion, circumventricular organ sensors reacting to osmotic pressure and angiotensin II, subserve genesis of thirst, volume regulation and behavioral effects of thirst avoidance.

Topics: Animals; Behavior; Brain; Dehydration; Humans; Hypothalamus; Neurons; Neurosecretory Systems; Osmolar Concentration; Osmoregulation; Perception; Pituitary Gland, Posterior; Thirst; TRPV Cation Channels; Vasopressins; Water Deprivation; Water-Electrolyte Balance

Reliable data at population level are essential to firmly establish links between fluid intake, hydration and health, investigate dose-response relationships and develop meaningful public health strategies or reference intake values. However, limited research exists regarding the most appropriate methodology for assessing beverage or total fluid intake (TFI). To date, methodologies have been developed to assess food and nutrient intake without due consideration of water or fluid intake behavior. A recent crossover study showed that a 24-hour food recall significantly underestimated mean TFI by 382 ml (95% CI 299-465) compared with a fluid specific 7-day record. The authors postulated that this average difference was mainly the result of missed drinking acts between meals a 24-hour recall was used. Using a 7-day record administered in paper form or on-line has also been shown to lead to a significantly different mean TFI of 129 ml. Therefore, the choice of methodology might result in measurement errors that limit between-survey or between-country comparisons. Such errors may contribute to variations in estimates of TFI that cannot be explained by differences in climate, physical activity or cultural habits. A recent survey confirmed the variation in methodologies used in European national dietary surveys. Since these surveys form the basis for setting adequate intakes for total water intake, measurement error between surveys should be limited, highlighting the need for the development of a consistent methodology that is validated for water and TFI estimation.

Topics: Arginine Vasopressin; Biomarkers; Cardiovascular Diseases; Dehydration; Drinking; Female; Glomerular Filtration Rate; Glycopeptides; Health Status; Humans; Hyperglycemia; Male; Metabolic Syndrome; Models, Biological; Prognosis; Renal Insufficiency, Chronic; Risk Factors; Urine; Vasopressins; Water-Electrolyte Balance

Circadian rhythms have evolved to anticipate and adapt animals to the constraints of the earth's 24-hour light cycle. Although the molecular processes that establish periodicity in clock neurons of the suprachiasmatic nucleus (SCN) are well understood, the mechanisms by which axonal projections from the central clock drive behavioural rhythms are unknown. Here we show that the sleep period in mice (Zeitgeber time, ZT0-12) is preceded by an increase in water intake promoted entirely by the central clock, and not motivated by physiological need. Mice denied this surge experienced significant dehydration near the end of the sleep period, indicating that this water intake contributes to the maintenance of overnight hydromineral balance. Furthermore, this effect relies specifically on the activity of SCN vasopressin (VP) neurons that project to thirst neurons in the OVLT (organum vasculosum lamina terminalis), where VP is released as a neurotransmitter. SCN VP neurons become electrically active during the anticipatory period (ZT21.5-23.5), and depolarize and excite OVLT neurons through the activation of postsynaptic VP V1a receptors and downstream non-selective cation channels. Optogenetic induction of VP release before the anticipatory period (basal period; ZT19.5-21.5) excited OVLT neurons and prompted a surge in water intake. Conversely, optogenetic inhibition of VP release during the anticipatory period inhibited the firing of OVLT neurons and prevented the corresponding increase in water intake. Our findings reveal the existence of anticipatory thirst, and demonstrate this behaviour to be driven by excitatory peptidergic neurotransmission mediated by VP release from central clock neurons.

Topics: Animals; Anticipation, Psychological; Biological Clocks; Dehydration; Drinking; Female; Male; Mice; Optogenetics; Organum Vasculosum; Post-Synaptic Density; Receptors, Vasopressin; Sleep; Synaptic Transmission; Thirst; Vasopressins; Water-Electrolyte Balance

Renal conservation (retention) of fluid might affect the outcome of hospital care and can be indicated by increased urinary concentrations of metabolic waste products. We obtained a reference material for further studies by exploring the prevalence of fluid retention in a healthy population.. Spot urine sampling was performed in 300 healthy hospital workers. A previously validated algorithm summarized the urine-specific gravity, osmolality, creatinine, and color to a fluid retention index (FRI), where 4.0 is the cut-off for fluid retention consistent with dehydration. In 50 of the volunteers, we also studied the relationships between FRI, plasma osmolality, and water-retaining hormones.. The cut-off for fluid retention (FRI ≥ 4.0) was reached by 38% of the population. No correlation was found between the FRI and the time of the day of urine sample collection, and the FRI was only marginally correlated with the time period spent without fluid intake. Volunteers with fluid retention were younger, generally men, and more often had albuminuria (88% vs. 34%, P < 0.001). Plasma osmolality and plasma sodium were somewhat higher in those with a high FRI (mean 294.8 vs. 293.4 mosmol/kg and 140.3 vs. 139.9 mmol/l). Plasma vasopressin was consistently below the limit of detection, and the plasma cortisol, aldosterone, and renin concentrations were similar in subjects with a high or low FRI. The very highest FRI values (≥ 5.0, N = 61) were always accompanied by albuminuria.. Fluid retention consistent with moderate dehydration is common in healthy staff working in a Swedish hospital.

Topics: Adult; Albuminuria; Aldosterone; Body Fluids; Creatinine; Cross-Sectional Studies; Dehydration; Female; Health Personnel; Humans; Hydrocortisone; Male; Multivariate Analysis; Osmolar Concentration; Renin; Specific Gravity; Urinalysis; Vasopressins

Water homeostasis is one of the body's most critical tasks. Physical challenges to the body, including exercise and surgery, almost always coordinate with some change in water handling reflecting the changing needs of the body. Vasopressin is the most important hormone that contributes to short-term water homeostasis. By manipulating vascular tone and regulating water reabsorption in the collecting duct of the kidneys, vasopressin can mediate the retention or loss of fluids quickly. In this study, we validated HumMod, an integrative mathematical model of human physiology, against six different challenges to water homeostasis with special attention to the secretion of vasopressin and maintenance of electrolyte balance. The studies chosen were performed in normal men and women, and represent a broad spectrum of perturbations. HumMod successfully replicated the experimental results, remaining within 1 standard deviation of the experimental means in 138 of 161 measurements. Only three measurements lay outside of the second standard deviation. Observations were made on serum osmolarity, serum vasopressin concentration, serum sodium concentration, urine osmolarity, serum protein concentration, hematocrit, and cumulative water intake following dehydration. This validation suggests that HumMod can be used to understand water homeostasis under a variety of conditions.

Topics: Body Water; Dehydration; Female; Fluid Therapy; Homeostasis; Humans; Kidney; Kidney Tubules, Collecting; Male; Models, Theoretical; Osmolar Concentration; Sodium; Urine; Vasopressins; Water-Electrolyte Balance

The addition of 25 mmol·L(-1) sodium to low alcohol (2.3% ABV) beer has been shown to enhance post exercise fluid retention compared with full strength (4.8% ABV) beer with and without electrolyte modification. This investigation explored the effect of further manipulations to the alcohol and sodium content of beer on fluid restoration following exercise. Twelve male volunteers lost 2.03 ± 0.19% body mass (mean ± SD) using cycling-based exercise. Participants were then randomly allocated a different beer to consume on four separate occasions. Drinks included low alcohol beer with 25 mmol·L-1 of added sodium [LightBeer+25], low alcohol beer with 50 mmol·L(-1) of added sodium [LightBeer+50], midstrength beer (3.5% ABV) [Mid] or midstrength beer with 25 mmol·L(-1) of added sodium [Mid+25]. Total drink volumes in each trial were equivalent to 150% of body mass loss during exercise, consumed over a 1h period. Body mass, urine samples and regulatory hormones were obtained before and 4 hr after beverage consumption. Total urine output was significantly lower in the LightBeer+50 trial (1450 ± 183 ml) compared with the LightBeer+25 (1796 ± 284 ml), Mid+25 (1786 ± 373 ml) and Mid (1986 ± 304 ml) trials (all p < .05). This resulted in significantly higher net body mass following the LightBeer+50 trial (-0.97 ± 0.17 kg) compared with all other beverages (LightBeer+25 (-1.30 ± 0.24 kg), Mid+25 (-1.38 ±0.33 kg) and Mid (-1.58 ±0.29 kg), all p < .05). No significant changes to aldosterone or vasopressin were associated with different drink treatments. The electrolyte concentration of low alcohol beer appears to have more significant impact on post exercise fluid retention than small changes in alcohol content.

Topics: Adult; Alcohol Drinking; Aldosterone; Athletes; Beer; Body Mass Index; Central Nervous System Depressants; Dehydration; Electrolytes; Ethanol; Exercise; Fluid Therapy; Humans; Male; Osmolar Concentration; Random Allocation; Sodium, Dietary; Sports Nutritional Physiological Phenomena; Vasopressins; Water-Electrolyte Balance; Young Adult

Dehydration, a condition that characterizes excessive loss of body water, is well known to be associated with acute renal dysfunction; however, it has largely been considered reversible and to be associated with no long-term effects on the kidney. Recently, an epidemic of chronic kidney disease has emerged in Central America in which the major risk factor seems to be recurrent heat-associated dehydration. This has led to studies investigating whether recurrent dehydration may lead to permanent kidney damage. Three major potential mechanisms have been identified, including the effects of vasopressin on the kidney, the activation of the aldose reductase-fructokinase pathway, and the effects of chronic hyperuricemia. The discovery of these pathways has also led to the recognition that mild dehydration may be a risk factor in progression of all types of chronic kidney diseases. Furthermore, there is some evidence that increasing hydration, particularly with water, may actually prevent CKD. Thus, a whole new area of investigation is developing that focuses on the role of water and osmolarity and their influence on kidney function and health.

Topics: Aldehyde Reductase; Central America; Dehydration; Disease Progression; Fluid Therapy; Fructokinases; Heat Exhaustion; Humans; Hyperuricemia; Metabolic Networks and Pathways; Osmolar Concentration; Recurrence; Renal Insufficiency, Chronic; Vasopressins

Neonatal hyponatraemia is common, and related to significant morbidity and mortality. We report a case of a preterm newborn (gestational age of 36 weeks) with hyponatraemia, and with a prenatal diagnosis of cleft lip and palate, with a normal fetal karyotype. On the seventh day of life, a biochemical evaluation for jaundice and mild signs of dehydration showed hyponatraemia of 124 mmol/L. Investigation showed normal adrenal and thyroid functions, plasma hyposmolality (258 mOsm/kg); high urinary sodium (73 mmol/L) and high urinary osmolality (165 mOsm/kg). Despite oral sodium supplementation and fludrocortisone treatment, sodium levels remained between 124 and 130 mmol/L. Cranial ultrasound, brain MRI and renal ultrasound were normal. The diagnosis of hyponatraemia was unpredicted and the investigation was suggestive of reset osmostat, a subtype of the syndrome of inappropriate secretion of antidiuretic hormone, characterised by a subnormal threshold for antidiuretic hormone secretion.

Topics: Anti-Inflammatory Agents; Dehydration; Fludrocortisone; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant, Newborn; Jaundice; Magnetic Resonance Imaging; Male; Osmolar Concentration; Premature Birth; Sodium; Vasopressins

Previous studies from our laboratory have shown that methysergide, a serotonergic antagonist, injected into the lateral parabrachial nucleus (LPBN) combined with a pre-load of 2 M NaCl, given by gavage, induces 0.3 M NaCl intake. The mechanisms involved in this paradoxical behavior are still unknown. In the present work, we investigated the effect of serotonergic blockade into the LPBN on hindbrain and hypothalamic activity, gastric emptying and arterial blood pressure in cell-dehydrated rats. Methysergide plus 2 M NaCl infused intragastrically or intravenously promoted 0.3 M NaCl intake in two-bottle tests. In cell-dehydrated rats with no access to fluids, methysergide compared to vehicle increased Fos immunoreactivity in the medial nucleus of the solitary tract, area postrema and non-oxytocinergic cells of the ventral portion of the hypothalamic paraventricular nucleus (PVN). There was no alteration in the number of neurons double-labeled for Fos-ir and oxytocin in the PVN and supraoptic nuclei. There was also no alteration in plasma oxytocin and vasopressin, or arterial pressure. In rats cell-dehydrated by i.v. 2 M NaCl, methysergide also did not change the amount of an intragastric load of 0.3 M NaCl retained in the stomach or intestine. The results suggest that methysergide injected into the LPBN of cell-dehydrated rat does not alter primary inhibitory signals that control sodium intake. The inhibitory signals blocked by methysergide in the LPBN possibly originated from activation of brain osmoreceptors, second order visceral/hormonal signals or a combination of both.

Topics: Animals; Area Postrema; Arterial Pressure; Dehydration; Disease Models, Animal; Gastric Emptying; Male; Methysergide; Neurons; Oxytocin; Parabrachial Nucleus; Proto-Oncogene Proteins c-fos; Rats, Sprague-Dawley; Saline Solution, Hypertonic; Serotonin Antagonists; Sodium Chloride, Dietary; Solitary Nucleus; Supraoptic Nucleus; Vasopressins

Dehydration activates the vasopressinergic system of the hypothalamus. We analyzed the effects of dehydration induced by water deprivation for 3 days on the activities of ERK1/2 and transcription factors, Elk1 and cAMP response element-binding protein (CREB) in vasopressinergic neurons, as well as the distribution and level of the motor protein, kinesin, in the hypothalamo-neurohypophyseal system. We showed that dehydration resulted in enhanced vasopressin (VP) expression and activation of CREB, and increased the activity of the MEK/ERK/Elk1 pathway in magnocellular neurons of the supraoptic nucleus. The activation of VP secretion was associated also with accumulation of phospho-ERK1/2 in the VP-ergic terminals of the posterior lobe of the pituitary. Analysis of the amount and distribution of kinesin and SNAP25, the proteins associated with transport and secretion, demonstrated that dehydration enhanced kinesin content in the perikarya of magnocellular neurons in the supraoptic nucleus and decreased kinesin and SNAP25 levels in the posterior pituitary. ERK1/2 and ERK1/2-dependent transcription factors, Elk1 and CREB, participate in the regulation of dehydration-evoked VP expression. We propose that ERK1/2 and kinesin participate in regulation of anterograde transport of VP dense core vesicles.

Topics: Animals; Cyclic AMP Response Element-Binding Protein; Dehydration; Gene Expression; Hypothalamus; Male; MAP Kinase Signaling System; Rats, Wistar; Vasopressins; Water Deprivation

Adequate hydration is essential for normal brain function and dehydration induces cognitive deterioration. In addition, dehydration has emerged as a stroke risk factor. However, it is unknown whether alterations in cerebrovascular regulation are responsible for these effects. To address this issue, C57Bl/6 mice were water deprived for 24 or 48 hours and somatosensory cortex blood flow was assessed by laser-Doppler flowmetry in a cranial window. Dehydration increased plasma osmolality and vasopressin levels, and suppressed the increase in blood flow induced by neural activity, by the endothelium-dependent vasodilator acetylcholine and the smooth muscle relaxant adenosine. The cerebrovascular dysfunction was associated with oxidative stress and cognitive deficits, assessed using the Y maze. The vasopressin 1a receptor antagonist SR49059 improved the dehydration-induced oxidative stress and vasomotor dysfunction. Dehydration upregulated endothelin-1 in cerebral blood vessels, an effect blocked by SR49059. Furthermore, the endothelin A receptor antagonist BQ123 ameliorated cerebrovascular function. These findings show for the first time that dehydration alters critical mechanisms regulating the cerebral circulation through vasopressin and oxidative stress. The ensuing cerebrovascular dysregulation may alter cognitive function and increase the brain's susceptibility to cerebral ischemia.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Brain; Cerebrovascular Circulation; Cognition Disorders; Dehydration; Endothelin-1; Male; Mice; Mice, Inbred C57BL; Osmolar Concentration; Oxidative Stress; Vasopressins; Water Deprivation

Arginine vasopressin (AVP) regulates water balance and blood pressure and plays a role in social behavioral processes. Healthy adult men as compared with women have higher blood levels of AVP and its C-terminal precursor peptide, copeptin.. The objective of the study was to investigate whether sexual disparity of copeptin is present at birth.. In 241 prospectively enrolled healthy newborn infants, 131 boys and 110 girls, plasma copeptin concentrations were measured at birth and on day 3 of life.. Multivariable linear regression analysis revealed stressful delivery (regression coefficient β = .569, P <0.001), acidosis (β = -.347, P < .001), and male gender (β = .132, P < .01) as independent determinants of copeptin at birth. In infants born without stress, that is by primary cesarean section (n = 81), male gender was the sole variable associated with copeptin (β = .286, P < .05), copeptin concentrations being higher in boys [median 5.5 pmol/L (interquartile range 4.4-10.2)] than in girls [4.8 pmol/L (interquartile range 3.6-5.8), P < .05]. At day 3 of life, copeptin was determined independently by postnatal physiological dehydration (β = .485; P < .001) and birth weight (β = .279; P < .01).. Sexual disparity of copeptin is already present at birth, indicating increased activation of the AVP system in newborn boys as compared with girls.

Topics: Dehydration; Delivery, Obstetric; Female; Gestational Age; Glycopeptides; Healthy Volunteers; Humans; Infant, Newborn; Linear Models; Male; Multivariate Analysis; Neurophysins; Pregnancy; Prospective Studies; Protein Precursors; Sex Characteristics; Stress, Physiological; Vasopressins

We present the novel urine collection method used during in-home interviews of a large population representative of older adults in the United States (aged 62-91, the National Social Life, Health and Aging Project). We also present a novel assay method for accurately measuring urinary peptides oxytocin (OT) and vasopressin (AVP), hormones that regulate social behaviors, stress, and kidney function.. Respondents in a randomized substudy (N = 1,882) used airtight containers to provide urine specimens that were aliquoted, stored under frozen refrigerant packs and mailed overnight for frozen storage (-80 °C). Assays for OT, AVP, and creatinine, including freeze-thaw cycles, were refined and validated. Weighted values estimated levels in the older U.S. population.. Older adults had lower OT, but higher AVP, without the marked gender differences seen in young adults. Mild dehydration, indicated by creatinine, specific gravity, acidity, and AVP, produced concentrated urine that interfered with the OT assay, yielding falsely high values (18% of OT). Creatinine levels (≥ 1.4 mg/ml) identified such specimens that were diluted to solve the problem. In contrast, the standard AVP assay was unaffected (97% interpretable) and urine acidity predicted specimens with low OT concentrations. OT and AVP assays tolerated 2 freeze-thaw cycles, making this protocol useful in a variety of field conditions.. These novel protocols yielded interpretable urinary OT and AVP values, with sufficient variation for analyzing their social and physiological associations. The problem of mild dehydration is also likely common in animal field studies, which may also benefit from these collection and assay protocols.

Topics: Age Factors; Aged; Aged, 80 and over; Aging; Creatinine; Dehydration; Female; Humans; Kidney; Longitudinal Studies; Male; Middle Aged; Oxytocin; Risk Factors; Sex Factors; Social Behavior; Stress, Psychological; United States; Urine Specimen Collection; Vasopressins

Topics: Adult; Dehydration; Diuresis; Drinking; Humans; Kidney; Kidney Diseases; Vasopressins; Water-Electrolyte Balance

The immunoglobulin heavy chain binding protein (BiP) is an endoplasmic reticulum (ER) chaperone that facilitates the proper folding of newly synthesized secretory and transmembrane proteins. Here we report that BiP mRNA was expressed in the supraoptic nucleus (SON) and paraventricular nucleus (PVN) of the hypothalamus in wild-type mice under basal conditions. Dual in situ hybridization in the SON and PVN demonstrated that BiP mRNA was expressed in almost all the neurons of arginine vasopressin (AVP), an antidiuretic hormone. BiP mRNA expression levels were increased in proportion to AVP mRNA expression in the SON and PVN under dehydration. These data suggest that BiP is involved in the homeostasis of ER function in the AVP neurons in the SON and PVN.

Topics: Animals; Corticotropin-Releasing Hormone; Dehydration; Endoplasmic Reticulum Chaperone BiP; Heat-Shock Proteins; Male; Mice; Mice, Inbred C57BL; Neurons; Oxytocin; Paraventricular Hypothalamic Nucleus; Supraoptic Nucleus; Up-Regulation; Vasopressins

Various lines of evidence indicate that astrocytes can undergo morphological changes that modify their relationship to adjacent neurons in response to physiological stimulation such as dehydration. Supraoptic (SON) and paraventricular (PVN) nuclei of hypothalamus represent obvious examples of activity-dependent neuro-astrocytic plasticity. In the present study, Meriones shawi is used as an animal model. Moreover, GFAP and vasopressin expressions are used as indicators successively of astrocytes and neuronal activations. In order to evaluate the reversibility of the neuro-astrocytic plasticity in SON and PVN, prolonged episode of water deprivation followed by episode of rehydration were examined. Hence, we studied the immunoreactivity in various hydration states: water ad libitum, dehydration, and rehydration of animals. Our results showed that dehydration of Meriones induced a significant decrease of GFAP immunoreactivity accompanied by a significant increase of AVP immunoreactivity, the latter concerns both cell bodies and fibers in the same hypothalamic nuclei SON and PVN. Conversely, rehydration of animals shows a reversible phenomenon leading a return of vasopressin and GFAP immunoreactivities to the control level. These results show that both astrocytes and vasopressin neurons display a remarkable structural and physiological plasticity, allowing to M. shawi, a great ability to support the hostile conditions in dry environment.

Topics: Animals; Dehydration; Desert Climate; Fluid Therapy; Gerbillinae; Glial Fibrillary Acidic Protein; Neuronal Plasticity; Paraventricular Hypothalamic Nucleus; Supraoptic Nucleus; Treatment Outcome; Vasopressins

Carbamazepine (CBZ) is a drug widely used in the therapy of epilepsy and mood disorders. One frequently observed side effect is hyponatraemia. The role of vasopressin in hyponatraemic action of CBZ is discussed controversially. In this study, we tested the influence of CBZ on water and salt homoeostasis in rat under different hydration states and under vasopressin 2 receptor (V2R) antagonism by satavaptan to elucidate the renal and vasopressin independent action of CBZ.. CBZ-treated rats were investigated on metabolic cages after (i) 6 day with ad libitum fluid intake, (ii) moderate water load and (iii) water restriction. The effect of satavaptan was tested in clearance experiments under continuous saline infusion in anaesthetized rats after CBZ pretreatment.. Compared to controls, CBZ induced a higher urinary flow rate which was most pronounced (20-fold) after water load and significantly elevated (2-fold) after 10-h water restriction. In addition, CBZ consistently increased renal sodium loss but failed to decrease plasma sodium concentration. In the presence of satavaptan, urinary flow and natriuresis were further increased by CBZ, while there was no differential effect on urea excretion and anion gap.. At the investigated dose (50 mg/kg body weight), CBZ did not induce hyponatraemia or antidiuresis in the rat. However, depending on the hydration state, it induced an increased water and electrolyte loss. Its enhanced influence on urinary flow and natriuresis in the presence of satavaptan suggests additional renal targets for CBZ, independent of vasopressin signalling.

Topics: Animals; Anticonvulsants; Antidiuretic Hormone Receptor Antagonists; Carbamazepine; Dehydration; Diuresis; Female; Hyponatremia; Kidney; Morpholines; Natriuresis; Rats; Rats, Wistar; Receptors, Vasopressin; Spiro Compounds; Vasopressins; Water-Electrolyte Balance

Supraoptic (SON) and paraventricular (PVN) nuclei are part of the hypothalamic-neurohypophysial system, they constitute the main source for vasopressin and they represent also obvious examples of activity-dependent neuroglial plasticity. Certain physiological conditions such as dehydration are accompanied by a structural remodeling of the neurons, their synaptic inputs and their surrounding glia. In the present work, an adult Meriones shawi (a rodent adapted to desert life) is used as an animal model. Using GFAP and vasopressin expressions as indicators successively of astrocytes and neuronal activations, the effect of a prolonged episode of water deprivation on the SON and PVN, hypothalamus nuclei were examined. We studied the immunoreactivity of GFAP and vasopressin in various hydration states (total deprivation of drinking water for 1 and 2months compared to hydrated animals). Prolonged dehydration produces an important decrease of GFAP immunoreactivity in both SON and PVN after 1 and 2months of water restriction. This decrease is accompanied by increased vasopressin immunoreactivity following the same periods of water deprivation. These findings may explain a real communication between vasopressin neurons and their surrounding astrocytes, thus the retraction of astrocytes and their processes is accompanied by an enhancement of vasopressin neuron density and their projecting fibers in response to this osmotic stress situation. Furthermore, these data could open further investigations concerning the possible involvement of the communication between astrocytes and vasopressin neurons in both PVN and SON in the regulation of Meriones hydrous balance and resistance to dehydration.

Topics: Animals; Astrocytes; Blotting, Western; Body Water; Dehydration; Gerbillinae; Glial Fibrillary Acidic Protein; Homeostasis; Immunohistochemistry; Midline Thalamic Nuclei; Nerve Fibers; Neuroglia; Neuronal Plasticity; Neurons; Osmolar Concentration; Supraoptic Nucleus; Vasopressins

Nasal obstruction is a risk factor in sleep-disordered breathing with a negative impact on the quality of life in humans. We investigated hydration changes produced by short term reversible, bilateral, nasal obstruction in young developing rat pups. Physiological parameters of growth (weight gain and gastric content weight) and dehydration were analyzed during two periods; during nasal obstruction at post-natal day 8 (days 9, 11 and 13), plus 7 and 90 days after recovery of nasal breathing (day 15 and adulthood). Body weight gain in oral breathing rat pups was slower compared to controls. Gastric weight was decreased significantly only in oral breathing rat pups on days 9 and 11 while plasma osmolality and vasopressin levels increased (indicators of dehydration). There were no differences between controls and treated rat pups by day 15, or at adulthood. Short term nasal obstruction-induced forced oral breathing, decreased gastric content which had a negative impact on growth and blood glucose concentration in the short term for female rat pups. Plasma corticosterone levels increased during the dehydration but were normal in males by 90 days. This could be a model for blocked nose syndrome in the newborn. Possible long term consequences on development are discussed.

Topics: Adrenal Cortex Hormones; Analysis of Variance; Animals; Animals, Newborn; Behavior, Animal; Blood Glucose; Body Weight; Dehydration; Female; Male; Mouth Breathing; Organ Size; Osmolar Concentration; Radioimmunoassay; Rats; Rats, Wistar; Sleep Apnea Syndromes; Stress, Psychological; Time Factors; Vasopressins; Weight Gain

In dehydrated rats, an early postingestive signal associated with the concentration of ingested fluid provides a signal that can inhibit neurohypophyseal vasopressin secretion. That inhibitory signal is not generated by the act of swallowing, as it is in dogs and many other animals, but by visceral osmoreceptors that presumably send a vagal signal to the nucleus of the solitary tract and the area postrema in the brain stem. In further contrast to dogs, the act of water ingestion does not provide an early signal inhibiting thirst in rats, but gastric emptying is so rapid that thirst can be satiated relatively quickly. When saline is consumed instead of water, thirst is inhibited by a different signal that results from the volume consumed and apparently is associated with gastrointestinal distension. These and other results emphasize the need to include gastric emptying of ingested fluid in considerations of water and Na(+) balance in rats.

Topics: Animals; Dehydration; Dogs; Drinking Behavior; Gastric Emptying; Osmolar Concentration; Rats; Vasopressins; Water-Electrolyte Balance

Klotho, a transmembrane protein, protease, and hormone mainly expressed in renal tissue counteracts aging. Overexpression of Klotho substantially prolongs the life span. Klotho deficiency leads to excessive formation of 1,25(OH)(2)D(3), growth deficit, accelerated aging, and early death. Aging is frequently paralleled by dehydration, which is considered to accelerate the development of age-related disorders. The present study explored the possibility that dehydration influences Klotho expression. Klotho transcript levels were determined by RT-PCR, and Klotho protein abundance was detected by Western blotting in renal tissue from hydrated and 36-h-dehydrated mice as well as in human embryonic kidney (HEK293) cells. Dehydration was followed by a significant decline of renal Klotho transcript levels and protein abundance, accompanied by an increase in plasma osmolarity as well as plasma ADH, aldosterone, and 1,25(OH)(2)D(3) levels. Antidiuretic hormone (ADH; 50 nM) and aldosterone (1 μM) significantly decreased Klotho transcription and protein expression in HEK293 cells. In conclusion, the present observations disclose a powerful effect of dehydration on Klotho expression, an effect at least partially mediated by enhanced release of ADH and aldosterone.

Topics: Aldosterone; Animals; Cholecalciferol; Dehydration; Down-Regulation; Female; Glucuronidase; HEK293 Cells; Humans; Klotho Proteins; Male; Mice; Osmolar Concentration; Vasopressins

Sweat Na(+) concentration ([Na(+)]) varies greatly among individuals and is particularly high in cystic fibrosis (CF). The purpose of this study was to determine whether excess sweat [Na(+)] differentially impacts thirst drive and other physiological responses during progressive dehydration via exercise in the heat. Healthy subjects with high-sweat [Na(+)] (SS) (91.0 ± 17.3 mmol/l), Controls with average sweat [Na(+)] (43.7 ± 9.9 mmol/l), and physically active CF patients with very high sweat [Na(+)] (132.6 ± 6.4 mmol/l) cycled in the heat without drinking until 3% dehydration. Serum osmolality increased less (P < 0.05) in CF (6.1 ± 4.3 mosmol/kgH(2)O) and SS (8.4 ± 3.0 mosmol/kgH(2)O) compared with Control (14.8 ± 3.5 mosmol/kgH(2)O). Relative change in plasma volume was greater (P < 0.05) in CF (-19.3 ± 4.5%) and SS (-18.8 ± 3.1%) compared with Control (-14.3 ± 2.3%). Thirst during exercise and changes in plasma levels of vasopressin, angiotensin II, and aldosterone relative to percent dehydration were not different among groups. However, ad libitum fluid replacement was 40% less, and serum NaCl concentration was lower for CF compared with SS and Control during recovery. Despite large variability in sweat electrolyte loss, thirst appears to be appropriately maintained during exercise in the heat as a linear function of dehydration, with relative contributions from hyperosmotic and hypovolemic stimuli dependent upon the magnitude of salt lost in sweat. CF exhibit lower ad libitum fluid restoration following dehydration, which may reflect physiological cues directed at preservation of salt balance over volume restoration.

Topics: Adult; Aldosterone; Angiotensin II; Body Weight; Case-Control Studies; Cystic Fibrosis; Dehydration; Exercise; Female; Hot Temperature; Humans; Male; Osmolar Concentration; Plasma Volume; Sodium; Sweat; Thirst; Vasopressins

Neuronal nitric oxide synthase (nNOS) has been reported to be up-regulated in the hypothalamic supraoptic nucleus (SON) during dehydration which in turn could increase nitric oxide (NO) production and consequently affect arginine vasopressin (AVP) secretion. The anteroventral third ventricle (AV3V) region has strong afferent connections with the SON. Herein we describe our analysis of the effects of an AV3V lesion on AVP secretion, and c-fos and nNOS expression in the SON following dehydration. Male Wistar rats had their AV3V region electrolytically lesioned or were sham operated. After 21 days they were submitted to dehydration or left as controls (euhydrated). Two days later, one group was anaesthetized, perfused and the brains were processed for Fos protein and nNOS immunohistochemistry (IHC). Another group was decapitated, the blood collected for hematocrit, osmolality, serum sodium and AVP plasma level analysis. The brains were removed for measurement of neurohypophyseal AVP content, and the SON was punched out and processed for nNOS detection by western blotting. The AV3V lesion reduced AVP plasma levels and c-fos expression in the SON following dehydration (P<0.05). Western blotting revealed an up-regulation of nNOS in the SON of control animals following dehydration, whereas such up-regulation was not observed in AV3V-lesioned rats (P<0.05). We conclude that the AV3V region plays a role in regulating the expression of nNOS in the SON of rats submitted to dehydration, and thus may affect the local nitric oxide production and the secretion of vasopressin.

Topics: Animals; Arginine Vasopressin; Dehydration; Hematocrit; Hypothalamus; Immunohistochemistry; Male; Nitric Oxide Synthase Type I; Osmolar Concentration; Pituitary Gland, Posterior; Proto-Oncogene Proteins c-fos; Rats; Rats, Wistar; Sodium; Supraoptic Nucleus; Third Ventricle; Vasopressins; Water Deprivation

In dehydrated animals, the antidiuretic hormone vasopressin (VP) is released from the nerve terminals of magnocellular neurons of the supraoptic nucleus (SON) and paraventricular nucleus (PVN) into the systemic circulation at the posterior pituitary. Increases in sodium (Na+)-level and osmolality in body fluids upon dehydration are reportedly sensed by a Na+-sensor and/or an osmosensor, respectively. However, it is still unknown whether both are involved in the regulation of production and/or release of VP. Na(x) is the cerebral Na+-level sensor and Na(x)-knockout mice do not stop ingesting salt even when dehydrated. Here we examined VP production/release in Na(x)-knockout mice, and found that they are normal in the VP response to dehydration or intraperitoneal-administration with hypertonic saline. In situ hybridization using an intron-specific probe showed that VP gene expression in the SON did not differ from wild-type mice when dehydrated. Also, there was no significant difference in the activity of subfornical organ neurons projecting to the SON between the two genotypes when stimulated by water deprivation. Furthermore, Na(x)-knockout mice showed a normal response in urine excretion to dehydration. All these results indicate that the information of Na+-level increase detected by Na(x) does not contribute to the control of VP production/release.

Topics: Animals; Dehydration; Genotype; Mice; Mice, Knockout; Neurons; Osmolar Concentration; RNA, Messenger; Saline Solution, Hypertonic; Sodium; Sodium Channels; Subfornical Organ; Supraoptic Nucleus; Urine; Vasopressins; Voltage-Gated Sodium Channels; Water Deprivation

Topics: Animals; Dehydration; Fluid Therapy; Humans; Nerve Net; Sleep; Suprachiasmatic Nucleus; Vasopressins

Polyuria is a symptom that appears in association with diabetes mellitus. Because sustained polyuria causes serious dehydration, it is believed that the body has a compensating mechanism to alleviate dehydration. In the present study, the role of renal aquaporin 2 (AQP2) in the compensating mechanism was investigated in KKAy mice, a type 2 diabetes model.. The renal AQP2 expression levels in KKAy mice aged between 5 and 24 weeks were determined using Western blotting. The hypothalamic vasopressin mRNA expression levels also were measured by real-time RT-PCR. Insulin was subcutaneously administered to 11-week-old KKAy mice twice a day for 7 days. After insulin treatment, the renal AQP2 protein expression and the hypothalamic vasopressin mRNA expression were measured.. The urinary volumes of 5- and 12-week-old KKAy mice were 1.5 ± 0.3 mL and 9.5 ± 1.2 mL, respectively. The inner medullary AQP2 protein expression of 12-week-old KKAy mice was approximately 2.5-fold higher than that of 5-week-old KKAy mice. The hypothalamic vasopressin mRNA expression of 12-week-old KKAy mice was approximately twice that of 5-week-old KKAy mice. Insulin treatment in KKAy mice resulted in a significant reduction in the plasma glucose level, urinary volume, and inner medullary AQP2 protein and hypothalamic vasopressin mRNA expression.. The present study demonstrated that AQP2 is a renal functional molecule of vasopressin that controls urinary volume and that AQP2 in the kidney increases to alleviate dehydration due to type 2 diabetes with polyuria.

Topics: Animals; Aquaporin 2; Blood Glucose; Blotting, Western; Dehydration; Diabetes Mellitus, Type 2; Disease Models, Animal; Gene Expression Regulation; Hypoglycemic Agents; Insulin; Male; Mice; Polyuria; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Vasopressins

Secretory-type Na-K-2Cl cotransporter (NKCC1) is known to play roles in both acid and sodium excretion, and is more abundant in dehydration. To determine the mechanisms by which dehydration stimulates NKCC1 expression, the effects of vasopressin, oxytocin and hyperosmolality on NKCC1 mRNA and protein expressions in the outer medullary collecting duct (OMCD) of rats were investigated using RT-competitive PCR and western blot analysis. Microdissected OMCD was incubated in isotonic or hypertonic solution, or with AVP or oxytocin for 60 min at 37 degrees C. Hyperosmolality induced by NaCl, mannitol or raffinose increased NKCC1 mRNA expression in OMCD by 130-240% in vitro. The stimulation of NKCC1 mRNA expression by NaCl was highest at 690 mosmol kg(-1) H(2)O and gradually decreased at higher osmolalities. The incubation of OMCD with AVP (10(-7) M) for 60 min increased NKCC1 mRNA expression by 100%. The administration of AVP to rats for 4 days using an osmotic mini-pump also increased NKCC1 mRNA and protein expressions in OMCD by 130%. In contrast, oxytocin (10(-7) M) did not stimulate the NKCC1 mRNA expression in OMCD in vitro. Chronic injection of oxytocin increased the NKCC1 mRNA expression by 36%. These data showed that hyperosmolality and vasopressin stimulate NKCC1 mRNA and protein expressions in rat OMCD. It is concluded that NKCC1 expression is regulated directly and indirectly by vasopressin.

Topics: Animals; Blotting, Western; Dehydration; DNA Primers; Dose-Response Relationship, Drug; Kidney Tubules, Collecting; Male; Microdissection; Oxytocin; Rats; Rats, Sprague-Dawley; Renal Agents; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Sodium-Potassium-Chloride Symporters; Solute Carrier Family 12, Member 2; Vasopressins; Water-Electrolyte Imbalance

Dehydration increases vasopressin (antidiuretic hormone) secretion from the posterior pituitary gland to reduce water loss in the urine. Vasopressin secretion is determined by action potential firing in vasopressin neurones, which can exhibit continuous, phasic (alternating periods of activity and silence), or irregular activity. Autocrine kappa-opioid inhibition contributes to the generation of activity patterning of vasopressin neurones under basal conditions and so we used in vivo extracellular single unit recording to test the hypothesis that changes in autocrine kappa-opioid inhibition drive changes in activity patterning of vasopressin neurones during dehydration. Dehydration increased the firing rate of rat vasopressin neurones displaying continuous activity (from 7.1 +/- 0.5 to 9.0 +/- 0.6 spikes s(1)) and phasic activity (from 4.2 +/- 0.7 to 7.8 +/- 0.9 spikes s(1)), but not those displaying irregular activity. The dehydration-induced increase in phasic activity was via an increase in intraburst firing rate. The selective -opioid receptor antagonist nor-binaltorphimine increased the firing rate of phasic neurones in non-dehydrated rats (from 3.4 +/- 0.8 to 5.3 +/- 0.6 spikes s(1)) and dehydrated rats (from 6.4 +/- 0.5 to 9.1 +/- 1.2 spikes s(1)), indicating that kappa-opioid feedback inhibition of phasic bursts is maintained during dehydration. In a separate series of experiments, prodynorphin mRNA expression was increased in vasopressin neurones of hyperosmotic rats, compared to hypo-osmotic rats. Hence, it appears that dynorphin expression in vasopressin neurones undergoes dynamic changes in proportion to the required secretion of vasopressin so that, even under stimulated conditions, autocrine feedback inhibition of vasopressin neurones prevents over-excitation.

Topics: Action Potentials; Animals; Cholecystokinin; Dehydration; Electrophysiology; Enkephalins; Female; Hypernatremia; Hyponatremia; Immunohistochemistry; In Situ Hybridization; Naltrexone; Narcotic Antagonists; Neurons; Oxytocin; Protein Precursors; Rats; Rats, Sprague-Dawley; Receptors, Opioid, kappa; RNA, Messenger; Vasopressins

The bHLH-PAS transcription SIM1 is required for the development of all neurons of the paraventricular nucleus (PVN) and supraoptic nucleus (SON) of the hypothalamus. Mice with a loss of Sim1 die within a few days of birth, presumably because of the lack of a PVN and SON. In contrast, mice with a decrease of Sim1 survive, are hyperphagic and become obese. The mechanism by which Sim1 controls food intake remains unclear. Here we show that the development of specific PVN and SON cell types is sensitive to Sim1 gene dosage. Sim1 haploinsufficiency reduces the number of vasopressin (AVP)- and oxytocin-producing cells in the PVN by about 50 and 80%, respectively, but does not affect the development of Crh, Trh and Ss neurons. A decrease of AVP-producing cells increases the sensitivity of Sim1 heterozygous mice to chronic dehydration. Moreover, retrograde labelling showed a 70% reduction of PVN neurons projecting to the dorsal vagal complex, raising the possibility that a decrease of these axons contributes to the hyperphagia of Sim1(+/-) mice. Sim1 haploinsufficiency is thus associated with a decrease of several PVN/SON cell types, which has the potential of affecting distinct homeostatic processes.

Topics: Animals; Basic Helix-Loop-Helix Transcription Factors; Brain Stem; Dehydration; Eating; Hypothalamus, Anterior; Male; Mice; Mice, Inbred C57BL; Mice, Inbred Strains; Mice, Transgenic; Neural Pathways; Neurons; Osmolar Concentration; Oxytocin; Paraventricular Hypothalamic Nucleus; Repressor Proteins; Sodium; Vasopressins

Neuronal activity regulated pentraxin (Narp) is a secreted, synaptic protein that has been implicated in modulating synaptic transmission. However, it is unclear how Narp secretion is regulated. Since we noted prominent Narp immunostaining in vasopressin neurons of the hypothalamus and in the posterior pituitary, we assessed whether it, like vasopressin, is released into the systemic circulation in an activity-dependent fashion. Consistent with this hypothesis, electron microscopic studies of the posterior pituitary demonstrated that Narp is located in secretory vesicles containing vasopressin. Using affinity chromatography, we detected Narp in plasma and found that these levels are markedly decreased by hypophysectomy. In addition, we confirmed that injection of a viral Narp construct into the hypothalamus restores plasma Narp levels in Narp knockout mice. In checking for activity-dependent secretion of Narp from the posterior pituitary, we found that several stimuli known to trigger vasopressin release, i.e. hypovolemia, dehydration and endotoxin, elevate plasma Narp levels. Taken together, these findings provide compelling evidence that Narp is secreted from vasopressin neurons in an activity-dependent fashion.

Topics: Adenoviridae; Animals; C-Reactive Protein; Chromatography, Affinity; Dehydration; DNA, Complementary; Genetic Vectors; Humans; Hypovolemia; Immunohistochemistry; Lipopolysaccharides; Mice; Mice, Knockout; Microscopy, Electron; Microscopy, Immunoelectron; Motor Activity; Nerve Tissue Proteins; Neurons; Pituitary Gland; Rats; Rats, Sprague-Dawley; Restraint, Physical; Stress, Psychological; Vasopressins

In a search for novel genes involved in the hypothalamic control of body energy homeostasis bioinformatic tools were applied. Analysis of the presence of structural features characteristic for secretory peptides was used as a first step in the identification of novel neuropeptides, and was followed by analysis of expression patterns. The gene product previously named TAFA5 was identified during this process. The overall mRNA expression pattern of TAFA5 was assessed using quantitative PCR on rat cDNA libraries. Furthermore, the brain mRNA and polypeptide expression patterns were examined in rats using in situ hybridization and immunohistochemistry. Our results substantiate previous findings that TAFA5 is mainly expressed in the central nervous system. Furthermore, we found TAFA5 mRNA to be highly expressed in the hypothalamic paraventricular nucleus (PVN) where it co-localized with vasopressin and oxytocin in magno- and parvocellular neurons. Immunohistochemical analysis revealed TAFA5 immunoreactivity in the PVN in accordance with the in situ hybridization data. Given the high levels of expression in the PVN, it was investigated whether TAFA5 mRNA levels were affected by fasting or dehydration. Interestingly, it was observed that TAFA5 mRNA was specifically down-regulated in the PVN following water deprivation. Based on our findings we suggest that TAFA5 may be involved in the regulation of fluid homeostasis.

Topics: Analysis of Variance; Animals; Computational Biology; Cytokines; Dehydration; Down-Regulation; Gene Expression; Male; Neuropeptides; Oxytocin; Paraventricular Hypothalamic Nucleus; Peptides; Rabbits; Rats; Rats, Sprague-Dawley; Time Factors; Vasopressins

1. This study presents a time course analysis of the messenger RNA (mRNA) levels of c-fos, vasopressin (VP), and oxytocin (OT) in the paraventricular (PVN) and supraoptic nucleus (SON), following acute and chronic dehydration by water deprivation. 2. Male Wistar rats were separated into five groups: nondehydrated (control group) and dehydrated for 6, 24, 48 and 72 h. Following water deprivation, animals were decapitated, their blood was collected for hematocrit, osmolality, and plasma sodium measurements, and brains were removed for dissection of both PVN and SON. 3. As expected, the hematocrit, osmolality, plasma sodium, and weight loss were increased after water deprivation. In SON, a significant increase in both VP and OT mRNA expression was observed 6 h after dehydration reaching a peak at 24 h and returning to basal levels of expression at 72 h. In the PVN, an increase in both VP and OTmRNA expression occurred 24 h after dehydration. At 72 h the VP and OT mRNA expression levels had decreased but they were still at higher levels than those detected in control animals. 4. These results suggest that SON is the first nucleus to respond to the dehydration stimulus. Additionally, we also observed an increase in c-fos mRNA expression in both PVN and SON 6 h after water deprivation, which progressively decreased 24, 48, and 72 h after the onset of water deprivation. Therefore, it is possible that c-fos may be involved in the modulation of VP and OT genes, regulating the mRNA expression levels on a temporally distinct basis within the PVN and SON.

Topics: Animals; Dehydration; Gene Expression; Hematocrit; Hypothalamus, Anterior; Male; Osmolar Concentration; Oxytocin; Paraventricular Hypothalamic Nucleus; Proto-Oncogene Proteins c-fos; Rats; Rats, Wistar; RNA, Messenger; Sodium; Vasopressins; Water Deprivation; Weight Loss

The hypothalamo-neurohypophyseal system (HNS) mediates neuroendocrine responses to dehydration through the action of the antidiuretic hormone vasopressin (VP). VP is synthesized as part of a prepropeptide in magnocellular neurons of the hypothalamic supraoptic nucleus (SON) and paraventricular nucleus. This precursor is processed during transport to axon terminals in the posterior pituitary gland, in which biologically active VP is stored until mobilized for secretion by electrical activity evoked by osmotic cues. During release, VP travels through the blood stream to specific receptor targets located in the kidney in which it increases the permeability of the collecting ducts to water, reducing the renal excretion of water, thus promoting water conservation. The HNS undergoes a dramatic function-related plasticity during dehydration. We hypothesize that alterations in steady-state protein levels might be partially responsible for this remodeling. We investigated dehydration-induced changes in the SON and pituitary neurointermediate lobe (NIL) proteomes using two-dimensional fluorescence difference gel electrophoresis. Seventy proteins were altered by dehydration, including 45 in the NIL and 25 in the SON. Using matrix-assisted laser desorption/ionization mass spectrometry, we identified six proteins in the NIL (four down, two up) and nine proteins in the SON (four up, five down) that are regulated as a consequence of chronic dehydration. Results for five of these proteins, namely Hsp1alpha (heat shock protein 1alpha), NAP22 (neuronal axonal membrane protein 22), GRP58 (58 kDa glucose regulated protein), calretinin, and ProSAAS (proprotein convertase subtilisin/kexin type 1 inhibitor), have been confirmed using independent methods such as semiquantitative Western blotting, two-dimensional Western blotting, enzyme-linked immunoassay, and immunohistochemistry. These proteins may have roles in regulating and effecting HNS remodeling.

Topics: Animals; Blotting, Western; Calbindin 2; Dehydration; Electrophoresis, Gel, Two-Dimensional; Hypothalamo-Hypophyseal System; Immunohistochemistry; Male; Mass Spectrometry; Nerve Tissue Proteins; Pituitary Gland; Protein Disulfide-Isomerases; Proteome; Proteomics; Rats; Rats, Sprague-Dawley; S100 Calcium Binding Protein G; Vasopressins

To test the effect of dehydration on brain atrial natriuretic peptide (ANP) concentrations in areas important to salt appetite, water balance and cardiovascular regulation, we subjected rats to dehydration and rehydration and measured ANP concentration in 18 brain areas, as well as all relevant peripheral parameters. Water deprivation decreased body weight, blood pressure, urine volume, and plasma ANP, while it increased urine and plasma osmolality, angiotensin II, and vasopressin. ANP greatly increased in 17 and 18 brain areas (all cut cerebral cortex) by 24 h. Rehydration for 12 h corrected all changes evoked by dehydration, including elevated ANP levels in brain. We conclude that chronic dehydration results in increased ANP in brain areas important to salt appetite and water balance. These results support a role for ANP as a neuroregulatory substance that participates in salt and water balance.

Topics: Angiotensin II; Animals; Atrial Natriuretic Factor; Blood Pressure; Body Weight; Brain; Cerebral Cortex; Dehydration; Male; Osmolar Concentration; Rats; Rats, Wistar; Thirst; Time Factors; Urine; Vasopressins; Water-Electrolyte Balance

Acute activation of the hypothalamic-pituitary-adrenal (HPA) axis releases glucocorticoids to maintain homeostasis, whereas prolonged exposure to elevated glucocorticoids has deleterious effects. Due to the potential benefits of limiting stress-induced glucocorticoid secretion, the present study uses drinking in dehydrated rats as a model to delineate mechanisms mobilized to rapidly inhibit HPA activity during stress. Using Fos expression as an indicator of neuronal activation, the effect of a single or repeated episode of dehydration-induced drinking on the activity of magnocellular and parvocellular neurons in the paraventricular nucleus (PVN) of the hypothalamus was examined. Adult male rats underwent a single episode or repeated (six) episodes of water restriction and were sacrificed before or after drinking water in the AM. Plasma osmolality, vasopressin (AVP), adrenocorticotropic hormone (ACTH) and corticosterone were elevated by water restriction and reduced after drinking in both models. Fos expression was elevated in AVP-positive magnocellular PVN neurons and AVP- and corticotropin releasing hormone (CRH)-positive parvocellular PVN neurons after water restriction. Fos expression was reduced in magnocellular AVP neurons after both models of restriction-induced drinking. In contrast, Fos expression did not change in AVP and CRH parvocellular neurons after a single episode of restriction-induced drinking, but was reduced after repeated episodes of restriction-induced drinking. These data indicate that drinking-induced decreases in glucocorticoids in dehydrated rats involve multiple factors including reduction in magnocellular release of vasopressin and reduction in parvocellular neuronal activity. The differential inhibition of PVN parvocellular neurons after repeated rehydration may reflect a conditioned response to repeated stress reduction.

Topics: Adrenocorticotropic Hormone; Animals; Conditioning, Psychological; Corticosterone; Dehydration; Drinking; Glucocorticoids; Hypothalamo-Hypophyseal System; Immunohistochemistry; Male; Neurons; Osmolar Concentration; Paraventricular Hypothalamic Nucleus; Proto-Oncogene Proteins c-fos; Rats; Rats, Sprague-Dawley; Stress, Physiological; Thirst; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Dehydration; Hypothalamo-Hypophyseal System; Pituitary Gland; Protein Disulfide-Isomerases; Proteomics; Rats; Vasopressins

We used neuronal nitric oxide synthase (nNOS) gene knockout mice to study the effects of catecholamines and neuronal nitric oxide on vasopressin expression in the hypothalamic neurosecretory centers. nNOS gene deletion did not change the level of vasopressin mRNA in the supraoptic or paraventricular nuclei. In contrast, vasopressin immunoreactivity was lower in nNOS deficient mice than in wild-type animals. Dehydration increased vasopressin mRNA levels and decreased vasopressin immunoreactivity in both wild-type and nNOS knockout mice, but these responses were more marked in the nNOS knockout mice. Treatment with alpha-mpt, a pharmacologic inhibitor of catecholamine synthesis, resulted in increased vasopressin mRNA levels in wild-type mice and in reduced vasopressin immunoreactivity in both wild-type and nNOS knockout mice. From these results, we conclude: (1) neuronal nitric oxide suppresses vasopressin expression under basal conditions and during activation of the vasopressinergic system by dehydration; (2) catecholamines limit vasopressin expression; (3) nNOS is required for the effects of catecholamines on vasopressin expression.

Topics: alpha-Methyltyrosine; Animals; Catecholamines; Dehydration; Enzyme Inhibitors; Gene Expression; Hypothalamus; Immunohistochemistry; In Situ Hybridization; Male; Mice; Mice, Knockout; Nitric Oxide; Nitric Oxide Synthase Type I; RNA, Messenger; Vasopressins

The hypothalamic-neurohypophyseal system (HNS) mediates neuroendocrine responses to dehydration through the actions of the antidiuretic hormone vasopressin (VP) and the natriuetic peptide oxytocin (OT). VP and OT are synthesised as separate prepropeptide precursors in the cell bodies of magnocellular neurones in the hypothalamic supraoptic nucleus (SON) and paraventricular nucleus, the axons of which innervate the posterior pituitary gland (PP). Dehydration evokes a massive release of both peptides into the circulation, and this is accompanied by a function-related remodelling of the HNS. Microarray studies on mRNAs differentially expressed in the SON revealed that transcripts encoding the Ywhag and Ywhaz isoforms of the 14-3-3 family of regulatory proteins, are increased in the rat SON by 3 days of water deprivation; findings that we have confirmed by the real-time polymerase chain reaction. Because there is no necessary proportionality between transcript and protein abundance, we next examined Ywhag and Ywhaz translation products throughout the HNS in parallel with 14-3-3 post-translational modification, which is known to be an important determinant of functional activity. Both proteins are robustly expressed in the SON in VP- and OT-containing neurones, but the abundance of neither changes with dehydration. However, the total level of Ywhaz protein is increased in the neurointermediate lobe of the pituitary (NIL, which includes the PP), in parallel with a basic post-translationally modified isoform, suggesting transport from the cell bodies of the SON of newly-synthesised protein and changes in its activity. The level of an acidic, probably phosphorylated, Ywhag isoform is down-regulated in the SON by dehydration, although total levels are unchanged. Finally, based on the presence of a phosphorylated 14-3-3 binding motif, we have identified a 14-3-3 binding partner, proteasome subunit, beta type 7, in the NIL. Thus, we suggest that, through complex transcriptional, and post-translational processes, 14-3-3 proteins are involved in the regulation or mediation of HNS plasticity following dehydration.

Topics: 14-3-3 Proteins; Animals; Cysteine Endopeptidases; Dehydration; Gene Expression Profiling; Gene Expression Regulation; Hypothalamo-Hypophyseal System; Male; Oligonucleotide Array Sequence Analysis; Oxytocin; Protein Isoforms; Proteome; Rats; Rats, Sprague-Dawley; Supraoptic Nucleus; Vasopressins; Water Deprivation

Central release of vasopressin (VP) by the magnocellular neuroendocrine cells (MNCs) responsible for systemic VP release is believed to be important in modulating the activity of these neurons during dehydration. Central VP release from MNC somata and dendrites is stimulated by both dehydration and pituitary adenylate cyclase activating polypeptide (PACAP). Although PACAP is expressed in MNCs, its potential role in the magnocellular response to dehydration is unexplored. The current study demonstrates that prolonged dehydration increases immunoreactivity for PACAP-27, PACAP-38, and the type I PACAP receptor in the supraoptic nucleus (SON) of the rat. In addition, PACAP stimulates local VP release in the euhydrated rat SON in vitro, and this effect is reduced by the PACAP receptor antagonist PAC(6-27) (100 nm), suggesting the participation of PACAP receptors. Concomitant with its effects on local VP release, PACAP also reduces basal glutamate and aspartate release in the euhydrated rat SON. Furthermore, somatodendritic VP release elicited by acute dehydration is blocked by PAC(6-27), suggesting that endogenous PACAP participates in this response. Consistent with this, RIA revealed that local PACAP-38 release within the SON is significantly elevated during acute dehydration. These results suggest that prolonged activation of hypothalamic MNCs is accompanied by up-regulation of PACAP and the type I PACAP receptor in these cells and that somatodendritic VP release in response to acute dehydration is mediated by activation of PACAP receptors by endogenous PACAP released within the SON. A potential role for PACAP in promoting efficient, but not exhaustive, systemic release of VP from MNCs during physiological challenge is discussed.

Topics: Adaptation, Physiological; Animals; Dehydration; Immunohistochemistry; Male; Neurosecretory Systems; Pituitary Adenylate Cyclase-Activating Polypeptide; Rats; Rats, Sprague-Dawley; Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type I; Signal Transduction; Supraoptic Nucleus; Vasopressins; Water-Electrolyte Balance

Western Australian agamid lizards are diverse and inhabit mesic to very arid areas of the state. Although reptilian kidneys are unable to elaborate hyperosmotic urine, we hypothesised that the renal system of lizards inhabiting arid areas would display an enhanced ability to conserve water under the control of the antidiuretic peptide hormone, arginine vasotocin (AVT). To examine this, the renal physiological and endocrine responses to osmotic challenge in three closely-related Australian agamid lizards inhabiting arid, semi-arid, and mesic environments were studied. The species studied were Pogona minor (mesic), Ctenophorus salinarum (semi-arid), and Ctenophorus nuchalis (arid). Circulating AVT was assayed and renal variables such as glomerular filtration rate (GFR), urine flow rate (V), and fractional reabsorption of filtrate FRH2O were measured in response to hypernatraemia, water load, and dehydration. Hypernatraemia and dehydration induced antidiuresis in all three species through similar mechanisms involving both glomerular and tubular responses. However, in salt-loaded P. minor the response was largely glomerular in nature, as FRH2O did not increase relative to the hydrated condition. The magnitude of the antidiuretic response was also greater in P. minor, indicating a greater sensitivity to osmotic challenge. Plasma concentrations of AVT were significantly correlated with FRH2O in P. minor (r2=0.38, P=0.025), but with GFR in C. nuchalis (r2=0.16, P=0.041). We found that the control and mechanisms of renal function among these lizards were largely similar, and there was little support for the hypothesis that arid lizards possess physiological adaptations not present in closely-related mesic lizards. Yet, differences remain in their response to hypernatraemia which may reflect the aridity of their different environments, or their varying habits.

Topics: Acclimatization; Animals; Body Water; Dehydration; Desert Climate; Environment; Kidney; Lizards; Osmolar Concentration; Receptors, Vasopressin; Vasopressins; Vasotocin; Water-Electrolyte Balance; Western Australia

The hypothalamoneurohypophyseal system (HNS) consists of the large peptidergic magnocellular neurons of the supraoptic hypo thalamic nucleus (SON) and the paraventricular hypothalamic nucleus (PVN), the axons of which course through the internal zone of the median eminence and terminate at blood capillaries of the posterior lobe of the pituitary gland. The HNS is a specialized brain neurosecretory apparatus responsible for the production of the antidiuretic peptide hormone vasopressin (VP). VP maintains water balance by promoting water conservation at the level of the kidney. Dehydration evokes a massive increase in the regulated release of VP from magnocellular neuron axon terminals in the posterior pituitary, which is accompanied by a plethora of changes in the morphology, electrophysiological properties, and biosynthetic and secretory activity of the HNS. We wish to understand this functional plasticity in terms of the differential expression of genes. We have therefore used microarrays to comprehensively catalog the genes expressed in the PVN, the SON and the neurointermediate lobe of the pituitary gland of control and dehydrated rats. Comparison of these gene lists has enabled us to identify transcripts that are regulated as a consequence of dehydration as well as RNAs that are enriched in the PVN or the SON. We suggest that these differentially expressed genes represent candidate regulators and effectors of HNS activity and remodeling.

Topics: Animals; Axons; Brain; Brain Mapping; Dehydration; Down-Regulation; Electrophysiology; Gene Expression Regulation; Hypothalamus; Kidney; Male; Oligonucleotide Array Sequence Analysis; Pituitary Gland, Posterior; Polymerase Chain Reaction; Rats; Rats, Sprague-Dawley; RNA; RNA, Messenger; Time Factors; Up-Regulation; Vasopressins; Water

Regulation of vasopressin (VP) and oxytocin (OT) secretion involves integration of neural signals from hypothalamic osmoreceptors, ascending catecholaminergic and peptidergic cell groups in the brain stem, and local and autoregulatory afferents. Neuropeptide Y (NPY) is one factor that stimulates the release of VP and OT from the supraoptic (SON) and paraventricular nuclei of the hypothalamus via activation of Y1 receptors (Y1R). The current studies were designed to assess the regulation and distribution of NPY Y1R expression in the SON of male rats that were either given 2% NaCl drinking water (24-72 h) or water deprived (48 h). Subjecting male rats to these conditions resulted in significant increases in both the number of cells expressing Y1R immunoreactivity (ir) and the amount of Y1R protein per cell within the SON. Y1R immunoreactivity was increased in the magnocellular but not medial parvocellular paraventricular nuclei, and Y1R mRNA levels were increased in the SON of salt-loaded rats. Subpopulations of both VP and OT cells in the hypothalamus express Y1R immunoreactivity and a greater percentage of VP-ir cells express Y1R after salt loading. To control for potential effects of dehydration-induced anorexia, a group of euhydrate animals was pair fed with animals consuming 2% NaCl. No detectable change in Y1R expression was observed in the SON of pair-fed animals, even though body weights were significantly lower than controls. These data demonstrate that NPY Y1R gene and protein expression are increased in the SON of salt-loaded and water-deprived animals and provide a mechanism whereby NPY can support VP/OT release during prolonged challenges to fluid homeostasis.

Topics: Animals; Blood; Body Weight; Dehydration; Gene Expression; Hypothalamus; Immunohistochemistry; Male; Neurons; Osmolar Concentration; Oxytocin; Paraventricular Hypothalamic Nucleus; Rats; Rats, Sprague-Dawley; Receptors, G-Protein-Coupled; Receptors, Neuropeptide; Sodium Chloride; Supraoptic Nucleus; Vasopressins; Water Deprivation

Reduction of vinculin occurs in the renal medulla under the long-lasting dehydration. The protein content measured in inner medulla of rats of the WAG line under hydration was 92.1 +/- 6.3 in relative units, but it was only 77.6 +/- 2.3 after a 3-day water deprivation. The vinculin content in the inner medullar layer from mutant rats of Brattleboro line incapable of synthesizing vasopressin is essentially higher: it is 188.9 +/- 8.5 in hydrated conditions and drops to 148.4 +/- 7.3 under a 3-day dehydration. The same high level of vinculin is in outer medulla from rats of Brattleboro line: 222.1 +/- 11.8 in hydrated animals and 174.9 +/- 11 after a 3-day dehydration. No differences were revealed in response of vinculin to alternative osmoregulating stimulation in cortex in both rat lines.

Topics: Animals; Dehydration; Kidney Medulla; Osmosis; Rats; Rats, Brattleboro; Species Specificity; Time Factors; Vasopressins; Vinculin; Water-Electrolyte Balance

A second vesicular glutamate transporter (VGLUT2) is detected in magnocellular neurons in the rat hypothalamus. The present study revealed what phenotype of neurons express VGLUT2 mRNA by the histological method. We found that most vasopressin (VP) neurons and several oxytocin (OT) neurons express VGLUT2 mRNA. VGLUT2 gene expression in VP and OT neurons is enhanced with osmotic challenges. In the neurohypophysis, VGLUT2-staining in OT terminals was reduced with osmotic stimulation. These results indicate that VGLUT2 is principally expressed in VP neurons and also in some OT neurons and that VGLUT2 in VP and OT neurons is involved in osmotic regulation.

Topics: Animals; Cell Shape; Dehydration; Male; Neurons; Osmolar Concentration; Oxytocin; Paraventricular Hypothalamic Nucleus; Rats; Rats, Sprague-Dawley; Salts; Supraoptic Nucleus; Up-Regulation; Vasopressins; Vesicular Glutamate Transport Protein 2; Water Deprivation

Drinking 2% NaCl decreases interleukin (IL)-1beta in the neural lobe and enhances IL-1 Type 1 receptor expression in magnocellular neurones and pituicytes. To quantify cytokine depletion from the neural lobe during progressive salt loading and determine whether the changes are reversible and correspond with stores of vasopressin (VP) or oxytocin (OT), rats were given water on day 0 and then 2% NaCl to drink for 2, 5, 8 or 5 days followed by 5 days of water (rehydration). Control rats drinking only water were pair-fed amounts eaten by 5-day salt-loaded animals. Animals were decapitated on day 8, the neural lobe frozen and plasma hormones analysed by radioimmunoassay (OT, VP) or enzyme-linked immunosorbent assay (IL-1beta). IL-1beta, VP and OT in homogenates of the neural lobe were quantified by immunocapillary electrophoresis with laser-induced fluorescence detection. Differences were determined by ANOVA, Tukey's t-test, Dunnett's procedure, Fisher's least significant difference and linear regression analysis. In response to salt-loading, rats lost body weight similar to pair-fed controls, drank progressively more 2% NaCl and excreted greater urine volumes. Plasma VP increased at days 2 and 8 of salt-loading, whereas osmolality, OT and cytokine were enhanced after 8 days with IL-1beta remaining elevated after rehydration. In the neural lobe, all three peptides decreased progressively with increasing duration of salt-loading (IL-1beta, r2 = 0.98; OT, r2 = 0.94; VP, r2 = 0.93), beginning on day 2 (IL-1beta; VP) or 5 (OT), with only VP replenished by rehydration. IL-1beta declined more closely (P < 0.0001; ANOVA interaction analysis) with OT (r2 = 0.96) than VP (r2 = 0.86), indicative of corelease from the neural lobe during chronic dehydration. Local effects of IL-1beta on magnocellular terminals, pituicytes and microglia in the neural lobe with activation of forebrain osmoregulatory structures by circulating cytokine may sustain neurosecretion of OT and VP during prolonged salt-loading.

Topics: Analysis of Variance; Animals; Dehydration; Interleukin-1beta; Male; Osmolar Concentration; Oxytocin; Pituitary Gland, Posterior; Pituitary Hormones, Posterior; Rats; Rats, Sprague-Dawley; Sodium Chloride, Dietary; Statistics, Nonparametric; Vasopressins; Water-Electrolyte Balance

Central vasopressin (VP) release from magnocellular neuroendocrine cells (MNCs) in the supraoptic nucleus (SON) occurs from their somata and dendrites within the SON several hours after acute dehydration, and is an important autoregulatory mechanism influencing the systemic release of VP from MNC terminals in the posterior pituitary. To begin to explore the impact of polychlorinated biphenyls (PCBs) on brain mechanisms of body fluid regulation, both central and systemic VP release in response to acute dehydration were assessed in adult male rats fed the commercial PCB mixture Aroclor 1254 (30 mg/kg/day) for 15 days. Water intake and body weight were recorded daily, and on day 15 rats were dehydrated by intraperitoneal injection of 3.5 M saline (controls received physiological saline) and sacrificed 4-6 h later. Intranuclear VP release was measured in SON tissue punches in vitro, and systemic VP release was measured in the same rats. SON prepared from dehydrated PCB-naive rats released significantly more VP than did SON from control rats (4.9 +/- 0.8 vs. 2.7 +/- 0.4 pg/ml/microg). In contrast, while Aroclor 1254 exposure had no effect on baseline water intake, weight gain, or plasma osmolality responses to dehydration in PCB-fed rats, the SON failed to respond with increased VP release during dehydration. Consistent with previous studies showing an inhibitory effect of central VP on plasma VP output, dehydrated PCB-fed rats had an exaggerated 863% increase in plasma VP over basal levels, compared to a 241% increase in PCB-naive rats, suggesting that the MNC system is subtly disrupted.

Topics: Animals; Central Nervous System; Chlorodiphenyl (54% Chlorine); Dehydration; Dendrites; Diet; Male; Neurosecretory Systems; Osmolar Concentration; Peripheral Nervous System; Rats; Signal Transduction; Supraoptic Nucleus; Vasopressins

Prostaglandins have an important role in renal salt and water reabsorption. PGE2 is the main kidney prostaglandin and is thought to be mainly produced in the kidney inner medulla (IM). There are indications that PGE2 synthesis in nephrogenic (NDI) and central (CDI) diabetes insipidus is altered. We hypothesize that the expression of the major PGE2 synthesis enzymes cyclooxygenases 1 and 2 (COX-1, COX-2) and membrane-associated PGE2 synthase (mPGES) is altered in the kidneys of rats with NDI and CDI. Wistar rats treated with lithium for 4 wk were used as the NDI model. One-half of the NDI model rats were additionally dehydrated for 48 h. Brattleboro (BB) rats that lack endogenous antidiuretic hormone were used as the CDI model. Expression and localization of COX-1, COX-2, and mPGES in IM, inner stripe of outer medulla (ISOM), and cortex were determined by immunoblotting and immunohistochemistry. In lithium-induced NDI, expression of COX-1, COX-2, and mPGES was markedly decreased in IM. In ISOM and cortex, COX-1 expression was marginally reduced and mPGES expression was unaltered. COX-2 expression was undetected in ISOM and marginally increased in cortex. Consistent with this, the density of COX-2-expressing cells in macula densa was significantly increased, indicating differential regulation of COX-2 in IM and cortex. Dehydration of NDI rats resulted in a marked increase in COX-2 immunolabeling in IM interstitial cells, and there was no significant change in COX-1 and mPGES expression in any kidney zone. Treatment of DDAVP in BB rats for 6 days resulted in a markedly increased expression of COX-1, COX-2, and mPGES in IM. In the cortex, there were no changes in the expression of COX-1 and mPGES, whereas COX-2 expression was decreased. These results identify markedly reduced expression of COX-1, COX-2, and mPGES in IM in lithium-induced NDI. Furthermore, there were major changes in the expression of COX-1, COX-2, and mPGES in rats with CDI.

Topics: Animals; Cyclooxygenase 1; Cyclooxygenase 2; Deamino Arginine Vasopressin; Dehydration; Diabetes Insipidus, Nephrogenic; Diabetes Insipidus, Neurogenic; Dinoprostone; Intramolecular Oxidoreductases; Kidney Concentrating Ability; Kidney Cortex; Kidney Medulla; Lithium; Male; Membrane Proteins; Polyuria; Prostaglandin-Endoperoxide Synthases; Rats; Rats, Brattleboro; Rats, Wistar; Renal Agents; Vasopressins; Water Deprivation

Evidence in rats suggests that central oxytocin (OT) signaling pathways contribute to suppression of food intake during dehydration (i.e., dehydration anorexia). The present study examined water deprivation-induced dehydration anorexia in wild-type and OT -/- mice. Mice were deprived of food alone (fasted, euhydrated) or were deprived of both food and water (fasted, dehydrated) for 18 h overnight. Fasted wild-type mice consumed significantly less chow during a 60-min refeeding period when dehydrated compared with their intake when euhydrated. Conversely, fasting-induced food intake was slightly but not significantly suppressed by dehydration in OT -/- mice, evidence for attenuated dehydration anorexia. In a separate experiment, mice were deprived of water (but not food) overnight for 18 h; then they were anesthetized and perfused with fixative for immunocytochemical analysis of central Fos expression. Fos was elevated similarly in osmo- and volume-sensitive regions of the basal forebrain and hypothalamus in wild-type and OT -/- mice after water deprivation. OT-positive neurons expressed Fos in dehydrated wild-type mice, and vasopressin-positive neurons were activated to a similar extent in wild-type and OT -/- mice. Conversely, significantly fewer neurons within the hindbrain dorsal vagal complex were activated in OT -/- mice after water deprivation compared with activation in wild-type mice. These findings support the view that OT-containing projections from the hypothalamus to the hindbrain are necessary for the full expression of compensatory behavioral and physiological responses to dehydration.

Topics: Animals; Anorexia; Blood Volume; Dehydration; DNA; Eating; Food Deprivation; Genotype; Hindlimb; Immunohistochemistry; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Oxytocin; Proto-Oncogene Proteins c-fos; Rhombencephalon; Vasopressins

Previous studies have shown decreased immunoreactive glial fibrillary acidic protein (GFAP) in the supraoptic nucleus (SON) when magnocellular neuroendocrine cells (MNCs) are activated by lactation or dehydration. This is thought to underlie structural plasticity of glial processes that occurs during these times. Here, we investigated how this apparent reduction in protein relates to GFAP mRNA expression in the dehydrated rat as visualized by in situ hybridization. Densitometry of silver grains in the SON revealed low levels of mRNA expression in control, 2-day dehydrated and 21-day rehydrated (R21) animals. Conversely, the SON from 7-day dehydrated (D7) subjects displayed significantly more silver grains. Thus, the pattern of GFAP mRNA expression is the inverse of what we previously observed for GFAP immunoreactivity in tissue sections of the SON. No differences in mRNA levels due to hydration state were seen in the lateral hypothalamic area, suggesting that increases in GFAP mRNA at D7 were specifically related to MNC activation. These data indicate a divergence in GFAP mRNA and protein expression in the SON.

Topics: Animals; Astrocytes; Dehydration; Down-Regulation; Gene Expression Regulation; Glial Fibrillary Acidic Protein; Hypothalamic Area, Lateral; Male; Neuronal Plasticity; Neurosecretory Systems; Pituitary Gland, Posterior; Rats; Rats, Sprague-Dawley; RNA, Messenger; Supraoptic Nucleus; Up-Regulation; Vasopressins; Water-Electrolyte Balance

The present study determined whether vasopressin (VP) secretion is inhibited by an oropharyngeal signal associated with swallowing fluids when dehydrated rats drink water, as it is when dehydrated dogs are used as experimental subjects (Thrasher, TN, Keil LC, and Ramsay DJ. Am J Physiol Regul Integr Comp Physiol 253: R509-R515, 1987). VP levels in systemic plasma (pVP) fell rapidly when rats drank water after overnight water deprivation. Systemic plasma Na+ concentration (pNa) also fell, but that change likely contributed little to the early inhibition of VP secretion. In contrast, consumption of water by dehydrated rats with an open gastric fistula had no effect on pVP, nor did consumption of isotonic saline by dehydrated rats; in neither case was pNa affected by fluid consumption. These findings provide no evidence that the act of drinking inhibits VP secretion in dehydrated rats. Thus some post-gastric effect of the ingested water seems to be responsible for the inhibitory signal. These results are consistent with previous suggestions that an early inhibitory stimulus for VP secretion in rats is provided by post-gastric visceral osmo- or Na+ receptors that sense the composition of the ingested fluid.

Topics: Animals; Dehydration; Drinking; Kinetics; Male; Osmolar Concentration; Rats; Rats, Sprague-Dawley; Sodium Chloride; Vasopressins; Water

Topics: Dehydration; Diabetes Insipidus, Nephrogenic; Humans; Hypernatremia; Polyuria; Vasopressins; Water Deprivation

Hypothalamic paraventricular and supraoptic nuclei are involved in the body fluid homeostasis. Especially vasopressin peptide and mRNA levels are regulated by hypo- and hyperosmolar stimuli. Other neuropeptides such as dynorphin, galanin and neuropeptide FF are coregulated with vasopressin. In this study neuropeptide FF and another RF-amide peptide, the prolactin-releasing peptide mRNA levels were studied by quantitative in situ hybridization after chronic salt loading, a laboratory model of chronic dehydration. The neuropeptide FF mRNA expressing cells virtually disappeared from the hypothalamic supraoptic and paraventricular nuclei after salt loading, suggesting that hyperosmolar stress downregulated the NPFF gene transcription. The neuropeptide FF mRNA signal levels were returned to control levels after the rehydration period of 7 days. No changes were observed in those medullary nuclei that express neuropeptide FF mRNA. No significant changes were observed in the hypothalamic or medullary prolactin-releasing peptide mRNA levels. Neuropeptide FF mRNA is drastically downregulated in the hypothalamic magnocellular neurons after salt loading. Other neuropeptides studied in this model are concomitantly coregulated with vasopressin: i.e. their peptide levels are downregulated and mRNA levels are upregulated which is in contrast to neuropeptide FF regulation. It can thus be concluded that neuropeptide FF is not regulated through the vasopressin regulatory system but via an independent pathway. The detailed mechanisms underlying the downregulation of neuropeptide FF mRNA in neurons remain to be clarified.

Topics: Animals; Dehydration; Drinking; Gene Expression; Hypothalamus, Anterior; Male; Neurons; Oligopeptides; Paraventricular Hypothalamic Nucleus; Rats; Rats, Sprague-Dawley; Receptors, G-Protein-Coupled; RNA, Messenger; Sodium Chloride; Solitary Nucleus; Thyrotropin-Releasing Hormone; Vasopressins

Dehydration is a classic homeostatic stressor in rats that leads to a series of endocrine responses including stimulation of the hypothalamo-pituitary-adrenal (HPA) axis. During the last decade, it has been well established that perinatal food restriction is associated with the onset of diseases in adults. Our previous demonstration of long-term alterations in HPA axis activity in both basal conditions and after a 72-hour dehydration period in 4-month-old rats exposed to a 50% maternal food restriction (FR50) in late gestation and lactation prompted us to investigate whether such perinatal undernutrition further affects HPA axis activity in mature animals. As previously described in 4-month-old rats under basal conditions, 8-month-old FR50 rats showed reduced body weight and an enhanced ratio between mineralocorticoid receptor (MR) and glucocorticoid receptor (GR) mRNA levels in the hippocampus, as well as increased pro-opiomelanocortin (POMC) mRNA levels in the adenohypophysis. In addition, numerous additional alterations appeared in mature rats. In the hypothalamus, levels of vasopressin (VP) mRNAs were increased both in the paraventricular nucleus (PVN) and in the supraoptic nucleus (SON). In the adenohypophysis, GR and prohormone-convertase 2 (PC2) mRNA levels were significantly increased, whereas prohormone-convertase 1 (PC1) mRNA was not affected by maternal undernutrition. Interestingly, undernourished animals exhibited high plasma levels of total and free corticosterone in spite of normal corticotropin (ACTH) levels, an indication that HPA basal activity is enhanced by maternal undernutrition in 8-month-old animals. Dehydration for 72 h induced a rise in ACTH plasma levels, but did not modify total and free corticosterone plasma levels in 8-month-old FR50 animals. In the adenopituitary, POMC mRNA levels were decreased after dehydration but PC1 mRNA levels were unaffected. The present study indicates that maternal food restriction during the perinatal period dramatically affects the activity of the HPA axis until the age of 8 months. We speculate that higher basal HPA activity and an inadequate HPA response after dehydration in mature animals may contribute to diseases such as hypertension, known to develop with aging in perinatally growth-restricted rats.

Topics: Adrenocorticotropic Hormone; Animals; Corticosterone; Dehydration; Food Deprivation; Hypothalamo-Hypophyseal System; In Situ Hybridization; Male; Pituitary-Adrenal System; Pro-Opiomelanocortin; Proprotein Convertase 1; Proprotein Convertase 2; Rats; Rats, Wistar; Receptors, Glucocorticoid; RNA, Messenger; Vasopressins

The time for reproduction in mammals largely depends on the availability of water and food in their habitat. Therefore, in regions where rains are limited to definite seasons of the year, mammals presumably will restrict their breeding correspondingly. But while mammals living in predictable ecosystems would benefit by timing their season to an ultimate predictable cue, such as photoperiod, in unpredictable ecosystems (e.g., deserts) they will need to use a more proximate signal. We suggest a mechanism by which water shortage (low water content in plants) could act as a proximate cue for ending the reproductive season. The golden spiny mouse (Acomys russatus), a diurnal rodent living in extreme deserts, may face an increased dietary salt content as the summer progresses and the vegetation becomes dry. Under laboratory conditions, increased diet salinity lead to reproductive hiatus in females, notable in imperforated vagina, and a significant decrease in the ovaries, uteri, and body masses. In females treated with vasopressin (VP), a hormone expressed during water stress, the uteri and body masses have decreased significantly, and the ovaries exhibited an increased number of atretic follicles. VP has also led to a significant decrease in relative medullary thickness (RMT) of the kidney. It is thus suggested that VP could act as a modulator linking the reproductive system with water economy in desert rodents, possibly through its act on the energetic pathways.

Topics: Adaptation, Physiological; Adrenal Glands; Animal Feed; Animals; Dehydration; Desert Climate; Female; Kidney; Muridae; Organ Size; Ovary; Reproduction; Seasons; Uterus; Vasopressins; Water-Electrolyte Balance

Adipsic hypernatraemia is an uncommon disorder in childhood caused by a defect in the osmoregulation of thirst, leading to impairment of water homeostasis and chronic hyperosmolality of body fluids. Adipsia is often associated with an abnormality in osmoregulated vasopressin secretion due to the close proximity of the hypothalamic osmoreceptors that control thirst with those regulating vasopressin secretion. Hypothalamic lesions of diverse aetiology (vascular abnormalities, neoplasms, granulomatous diseases, trauma etc.) have been described in this syndrome. We report a 12-year-old boy with evident weight loss due to hypernatraemic dehydration with a selective defect in osmoregulation of thirst and normal vasopressin secretion with no demonstrable structural lesion. To date, only six paediatric patients with this condition have been described in the literature.. Hypothalamic adipsic hypernatraemia syndrome must be suspected when a dehydrated patient denies thirst. The study of antidiuretic function is necessary because the osmoregulation of vasopressin secretion could be altered.

Topics: Brain; Child; Dehydration; Drinking; Humans; Hypernatremia; Hypothalamic Diseases; Magnetic Resonance Imaging; Male; Prognosis; Syndrome; Vasopressins; Water-Electrolyte Balance

The anteroventral region of the third ventricle (AV3V) is critical in mediating osmotic sensitivity. AV3V lesions increase plasma osmolality and block osmotic-induced vasopressin (VP) and oxytocin (OT) secretion. The aim was to evaluate the effects of AV3V lesions on neurosecretion under control/water replete conditions and after 48 h dehydration. The focus was on central peptidergic changes with measurement of OT and VP content in the hypothalamic paraventricular (PVN) and supraoptic (OT) regions and the posterior pituitary. AV3V-lesioned rats exhibited an elevated plasma osmolality and higher OT content in SON and PVN. There was an increase in VP content in PVN, but no change in SON. As predicted, the plasma peptide response to dehydration was absent in lesioned animals. However, dehydration produced depletion in posterior pituitary VP in lesioned animals with no change in OT. No changes in nuclear VP and OT levels were seen after dehydration. These results demonstrate that AV3V lesions alter the VP and OT neurosecretory system, seen as a blockade of osmotic-induced release and an increase in basal nuclear peptide content. The data indicate that interruption of the osmotic sensory system affects the central neurosecretory axis, resulting in a backup in content and likely changes in synthesis and processing.

Topics: Animals; Brain Diseases; Dehydration; Hypothalamo-Hypophyseal System; Male; Microdissection; Osmolar Concentration; Osmotic Pressure; Oxytocin; Paraventricular Hypothalamic Nucleus; Pituitary-Adrenal System; Radioimmunoassay; Rats; Rats, Wistar; Supraoptic Nucleus; Third Ventricle; Vasopressins; Water; Water-Electrolyte Balance

Topics: Acidosis; Ammonium Chloride; Animals; Aquaporin 2; Aquaporins; Dehydration; Disease Models, Animal; Vasopressins

In order to investigate the effects of centrally administered ANP on plasma ADH, aldosterone and corticosterone levels as well as on blood pressure and on heart rate, 20 male New Zealand White (NZW) rabbits were used. Measurements were made on restrained conscious animals one week after the implantation of an indwelling intracerebroventricular (icv) cannula and two indwelling intravascular catheters (intracarotid and intrajugular). Animals were classified into two main groups, those with water available ad libitum ("euhydrated" group) and those who were dehydrated for 24 h ("dehydrated" group) before blood pressure and heart rate recordings and blood sampling for hormonal determination. Each group's individuals were divided into two subgroups of five animals each. Blood samples were collected at 0 min (control) and 30, 60, 90, 120 min following icv administration of 25 microl of either artificial cerebrospinal fluid (aCSF) (subgroups "aCSF") or human (h) ANP (1 microg) in aCSF (25 microl) (subgroups "hANP"). Blood pressure and heart rate were also recorded at the same times. Plasma ADH, aldosterone and corticosterone concentrations were determined using RIA. The results were analysed by analysis of variance (ANOVA). Blood pressure and heart rate values were unaffected by water deprivation or by ANP administration. Mean plasma corticosterone levels at all times (30-120 min) were significantly higher (p<0.001) than those at 0 min time. Plasma corticosterone levels in the "dehydrated+aCSF" group were significantly higher (p<0.05) than in each of the other groups ("dehydrated+hANP", "euhydrated+aCSF", "euhydrated+hANP"). Plasma corticosterone levels in each of those other groups did not differ significantly from one another. Dehydration resulted in a tendency to increase in aldosterone levels (p<0.07), and icv administration of hANP tended (p<0.08) to prevent in the "dehydrated+hANP" experimental group the increase in aldosterone levels observed in the control "dehydrated+aCSF" group from 30 to 120 min. Dehydration resulted in an increase in ADH levels (p<0.0001), and icv administration of hANP prevented (p<0.05) in "dehydrated+hANP" experimental group the increase in ADH levels observed in the control "dehydrated+aCSF" group from 90 to 120 min. The increase of corticosterone and ADH and the tendency towards increase in aldosterone in the control dehydrated groups could possibly be due to the combined stress stimulus of dehydration and restriction in the rest

Topics: Aldosterone; Animals; Atrial Natriuretic Factor; Blood Pressure; Corticosterone; Dehydration; Heart Rate; Humans; Injections, Intraventricular; Male; Osmolar Concentration; Rabbits; Restraint, Physical; Vasopressins

Physiological activation of the hypothalamo-neurohypophyseal system (HNS) by dehydration results is a massive release of vasopressin (VP) from the posterior pituitary. This is accompanied by a functional remodeling of the HNS. In this study we used cDNA arrays in an attempt to identify genes that exhibit differential expression in the hypothalamus following dehydration. Our study revealed nine candidate genes, including interleukin-6 (IL-6) as a putative novel secretory product of HNS worthy of further analysis. In situ hybridization and immunocytochemistry confirmed that IL-6 is robustly expressed in the supraoptic (SON) and the paraventricular (PVN) nuclei of the hypothalamus. By double staining immunofluorescence we showed that IL-6 is largely co-localized with VP in the SON and PVN. In situ hybridization, immunocytochemistry, and Western blotting all revealed IL-6 up-regulation in the SON and PVN following dehydration, thus validating the array data. The same dehydration stimulus resulted in an increase in IL-6 immunoreactivity in the axons of the internal zone of the median eminence and a marked reduction in IL-6-like material in the posterior pituitary gland. We thus suggest that IL-6 takes the same secretory pathway as VP and is secreted from the posterior pituitary following a physiological stimulus.

Topics: Animals; Axons; Blotting, Western; Dehydration; Fluorescent Antibody Technique; Gene Expression; Gene Expression Regulation; Hypothalamus; Immunohistochemistry; In Situ Hybridization; Interleukin-6; Male; Median Eminence; Oligonucleotide Array Sequence Analysis; Paraventricular Hypothalamic Nucleus; Pituitary Gland, Posterior; Rats; Rats, Sprague-Dawley; RNA, Messenger; Supraoptic Nucleus; Vasopressins

The aim of this study was to assess our hypothesis that the release of antidiuretic hormone (ADH), the renal concentrating response to ADH, or both is decreased by prolonged cold exposure. Six groups (n = 6/group) of rats were used. Three groups were exposed to cold (5 degrees C), whilethe remaining three groups were kept at room temperature (25 degrees C). It was found that urine osmolality decreased significantly and serum osmolality increased significantly during cold exposure. The ratio of water/food intake was not affected by prolonged cold exposure. However, prolonged cold exposure increased the ratio of urine output/food intake in the cold-exposed rats, indicating that more urine flow is required by the cold-exposed rats to excrete the osmotic substance at a given food intake. The difference between water intake and urine output decreased significantly in the cold-exposed rats. Thus, prolonged cold exposure increases water loss from excretion. Renal concentrating responses to 24-h dehydration and Pitressin were decreased significantly in the cold-exposed rats. Plasma ADH levels remained unchanged, but renal ADH receptor (V2 receptor) mRNA was decreased significantly in the cold-exposed rats. The results strongly support the conclusion that cold exposure increases excretive water loss, and this may be due to suppression of renal V2 receptors rather than inhibition of ADH release.

Topics: Animals; Arginine Vasopressin; Body Water; Cold Temperature; Dehydration; Diuresis; Drinking; Eating; Kidney; Male; Osmolar Concentration; Rats; Rats, Sprague-Dawley; Receptors, Vasopressin; Renal Agents; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Time Factors; Vasopressins; Water-Electrolyte Balance

We have tested the hypothesis that 3', 5'-cyclic adenosine monophosphate (cAMP)-dependent protein kinase A (PKA) is involved in the regulation of the vasopressin (VP) gene in the magnocellular neurons of the paraventricular nucleus (PVN) of the osmotically challenged rat. An adenoviral vector expressing a potent peptide inhibitor of PKA, Ad.CMV.PKIalpha, was demonstrated to be highly efficient in vitro. Ad.CMV.PKIalpha was then introduced into the PVN of rats bearing a VP reporter transgene (3-VCAT-3) consisting of the VP structural gene containing an epitope reporter in exon III, flanked by 3 kb of upstream and 3 kb of downstream sequence Robust transgene expression is seen in VP neurons of the PVN, and this increases following 72 h of dehydration. Ad.CMV.PKIalpha significantly blunted 3-VCAT-3 expression in the osmotically stimulated PVN. Our evidence suggests that PKA mediates changes in VP gene expression in response to dehydration through sequences contained within the 3-VCAT-3 transgene.

Topics: Adaptor Proteins, Signal Transducing; Animals; Animals, Genetically Modified; Carrier Proteins; Cell Line; Cyclic AMP-Dependent Protein Kinases; Dehydration; Female; Gene Expression Regulation; Genes, Reporter; Genetic Vectors; Hypothalamo-Hypophyseal System; Male; Paraventricular Hypothalamic Nucleus; Rats; Rats, Sprague-Dawley; Recombinant Fusion Proteins; Transgenes; Vasopressins; Water-Electrolyte Balance

Plasma vasopressin (VP) and corticosterone have each been shown to be rapidly suppressed after drinking in different models of osmotic stimulation in rats; however, no causal relationship between these responses has been investigated. Studies were performed to determine if plasma VP and corticosterone are reduced in parallel after drinking and if manipulation of plasma VP affects plasma, ACTH corticotropins and corticosterone in a model of water restriction. A strong correlation between changes in plasma VP and corticosterone, but not between plasma ACTH and corticosterone, was observed after drinking induced by 6 days of water restriction. Similarly, ingestion of isotonic saline resulted in a biphasic VP response that was paralleled by adrenal and plasma corticosterone, but not by plasma ACTH. Administration of an immunoneutralizing antibody directed against VP resulted in a rapid decrease in plasma corticosterone, but not ACTH, in water-restricted rats, but not in rats receiving water ad libitum. These data suggest that during dehydration, elevated plasma VP can stimulate the production of corticosterone by the adrenal, independently of ACTH. Moreover, they support the hypothesis that the decline in corticosterone after restriction-induced drinking is due, in part, to a decline in plasma VP.

Topics: Adrenal Glands; Adrenocorticotropic Hormone; Animals; Corticosterone; Dehydration; Drinking; Isotonic Solutions; Male; Osmolar Concentration; Rats; Rats, Sprague-Dawley; Sodium Chloride; Vasopressins; Water Deprivation

Galanin (Gal) as a neuropeptide with widespread distribution in the central nervous system may be involved in the mechanisms of vasopressin (AVP) and oxytocin (OT) release from the hypothalamo-neurohypophysial system. Vasopressin and oxytocin content in the hypothalamus and neurohypophysis as well as plasma level of both neurohormones were studied after galanin treatment in euhydrated and dehydrated rats. In not dehydrated rats intracerebroventricular (i.c.v.) injections of Gal did not affect the hypothalamic and neurohypophysial OT content, however, distinctly increased plasma OT concentration. In the same animals Gal diminished the hypothalamic AVP content but was without the effect on neurohypophysial AVP storage; plasma AVP level then raised. Galanin, administered i.c.v. to rats deprived of water, distinctly inhibited AVP and OT release from the hypothalamo-neurohypophysial system. Simultaneously, plasma AVP and OT level was significantly diminished after Gal treatment in dehydrated rats. These results suggest that modulatory effect of galanin on vasopressin and oxytocin release depends on the actual state of water metabolism. Gal acts as an inhibitory neuromodulator of AVP and OT secretion under conditions of the dehydration but stimulates this process in the state of equilibrated water metabolism.

Topics: Animals; Body Water; Dehydration; Drug Administration Schedule; Galanin; Hypothalamo-Hypophyseal System; Hypothalamus; Injections, Intraventricular; Male; Oxytocin; Pituitary Gland, Posterior; Radioimmunoassay; Rats; Rats, Wistar; Vasopressins

The intrarenal distribution of actinin and tropomyosin was studied by western blot analysis in various functional conditions. It was found that actinin content is always higher in cortex than in medulla. The highest tropomyosin content was revealed in outer medulla, but it is more than twice higher in rats of mutant Brattleboro line versus hydrated normal WAG rats. This ratio rises up to 46.12 +/- 2.14 versus 13.83 +/- 0.66 (in relative units) for rats being under dehydration that maximally activated vasopressin secretion in normal WAG rats.

Topics: Actinin; Animals; Blotting, Western; Dehydration; Kidney; Kidney Cortex; Kidney Medulla; Rats; Rats, Brattleboro; Rats, Inbred Strains; Renal Agents; Tissue Distribution; Tropomyosin; Vasopressins

Our objective was to test the hypothesis that the cGMP signal-transduction mechanism mediates nitric oxide's (NO) modulation of oxytocin (OT) and vasopressin (VP) secretion from the hypothalamo-neurohypophysial system. Three studies were conducted in adult male Sprague-Dawley rats: (1a) Euhydrated rats received an intracerebroventricular (icv) infusion (1 microl/min for 30 min) of artificial cerebrospinal fluid (aCSF), vehicle (2.6% dimethyl sulfoxide [DMSO]) or 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ) (0.05 microg/microl), an inhibitor of soluble guanylyl cyclase (sGC). ODQ did not affect basal levels of plasma VP or OT; (1b) Rats dehydrated for 24 h received aCSF or 8-Br-cGMP (icv), a membrane-permeable analog of cGMP, and plasma hormones were measured 2 min later. 8-Br-cGMP did not significantly change VP or OT levels; (2) Rats ingested water or 2% NaCl for 4 days, and NO synthase (NOS) and sGC activities were measured in posterior pituitaries, the anatomical site of hormone secretion. Salt loading enhanced (P < 0.001) production of [(14)C]citrulline, the coproduct of NO synthesis, without altering cGMP; (3) One SON was microdialyzed with [(14)C]arginine and NOS and sGC activities were quantified in microdialysates during intravenous (iv) infusion of isotonic or hypertonic saline in awake and anesthetized rats. In awake rats, [(14)C]citrulline recovery, but not cGMP, increased (P < 0.05) during intravenous infusion of both isotonic and hypertonic solutions, and after insertion of microdialysis probe itself. In anesthetized rats, however, where basal NOS activity is low, intravenous infusion of hypertonic, but not isotonic solution, increased [(14)C]citrulline recovery without affecting cGMP. Thus, in the forebrain, neither NO produced basally nor during osmotic stimulation depends on cGMP to modulate plasma vasopressin and oxytocin secretion.

Topics: Animals; Citrulline; Consciousness; Cyclic GMP; Dehydration; Enzyme Inhibitors; Guanylate Cyclase; Hypothalamo-Hypophyseal System; Injections, Intraventricular; Isotonic Solutions; Male; Microdialysis; Nitric Oxide; Nitric Oxide Synthase; Oxytocin; Pituitary Gland, Posterior; Rats; Rats, Sprague-Dawley; Saline Solution, Hypertonic; Signal Transduction; Sodium Chloride; Supraoptic Nucleus; Vasopressins; Water-Electrolyte Balance

Dehydration, a classic homeostatic stressor in rats, leads to a series of well characterized endocrine responses including stimulation of the hypothalamo-pituitary-adrenal (HPA) axis. In this study, the hypothesis to be tested was that a 50% maternal food restriction (FR50) in late gestation and lactation may have long-term repercussions on HPA axis responsiveness to dehydration in offspring. For this purpose, we studied HPA axis activity in 4-month-old control (C) and perinatally malnourished male rats after a 72-hour water deprivation period. Furthermore, we investigated the long-lasting effects of perinatal maternal malnutrition on the basal activity of the HPA axis. Under basal conditions, rats exposed to perinatal malnutrition showed reduced body weight, enhanced mineralocorticoid receptor (MR) mRNA levels in CA2 and CA3 hippocampal areas, but decreased glucocorticoid receptor (GR) mRNA levels in CA1, CA3 and dentate gyrus (DG) areas. In contrast, the levels of corticotropin-releasing hormone (CRH) and vasopressin (VP) mRNAs in the hypothalamic paraventricular nucleus (PVN) as well as of VP mRNA in the supraoptic nucleus (SON) were unaffected by maternal undernutrition. Expression of proopiomelanocortin (POMC) in the adenohypophysis was significantly enhanced, whereas prohormone convertase-1 (PC1) was not affected. Perinatal malnutrition reduced absolute adrenal weight but did not affect circulating levels of adrenocorticotropin (ACTH), corticosterone and free corticosterone as well as corticosteroid-binding globulin (CBG) binding capacity. Seventy-two hours of dehydration induced a decrease in body weight and CRH mRNA levels in PVN of controls as well as of FR50 rats, but also led to a rise in plasma corticosterone and free corticosterone without changing CBG binding capacity. Dehydration also induced an increase in adenopituitary POMC (C) and PC1 (FR50), PVN and SON VP (C) and GR in CA1 hippocampal area (FR50) mRNA levels and plasma ACTH (C), but a decrease in MR in DG (C) and GR in CA3 and DG (C) mRNA levels. We conclude that maternal food restriction during the perinatal period affects (1) the adult basal activity of the HPA axis with mainly opposite effects on hippocampal MR and GR gene expression and an increase in adenopituitary POMC gene expression, and (2) the responsiveness to water deprivation in adults. In the latter case, the rise in plasma ACTH levels, adenopituitary POMC gene expression, hypothalamic VP gene expression, and the decreas

Topics: Adrenal Glands; Animals; Animals, Newborn; Aspartic Acid Endopeptidases; Blood; Body Weight; Dehydration; Female; Food Deprivation; Hormones; Hypothalamo-Hypophyseal System; Hypothalamus; Male; Organ Size; Pituitary Gland, Anterior; Pituitary-Adrenal System; Pregnancy; Prenatal Exposure Delayed Effects; Pro-Opiomelanocortin; Proprotein Convertases; Rats; Rats, Wistar; Receptors, Glucocorticoid; Receptors, Mineralocorticoid; Transcortin; Vasopressins

Our previous studies indicated that in the human paraventricular (PVN) and supraoptic (SON) nuclei, tyrosine hydroxylase (TH)--the first and rate-limiting enzyme in catecholamine synthesis--is localized mainly in magnocellular neurons and that antemortem factors regulate its expression. The purpose of the present study was to investigate the distribution of TH-immunoreactive (TH-IR) perikarya of the hypothalami of a large sample of well-documented adult subjects without neurological, psychiatric or endocrinological disease in order to identify factors that could regulate the expression of TH in the human neurosecretory neurons. Our material consisted of the hypothalami of 38 subjects studied immunohistochemically for TH using the peroxidase-antiperoxidase method. Striking individual differences were observed among the subjects studied concerning the number and distribution of TH-IR perikarya within the PVN and SON. These differences were evident throughout the entire rostrocaudal length of the hypothalamus and appeared to be related neither to the age or sex of the subjects nor to the postmortem interval or staining procedures. In the sample studied, a large number of TH-IR perikarya were observed specifically in all subjects that had suffered from right-sided heart failure due to pulmonary hypertension, liver cirrhosis or dehydration. In all the above illnesses, increased production and secretion of vasopressin (VP) are reported to occur due to a decrease in 'effective' blood volume or to osmotic stimulation. We conclude that somatic illnesses leading to prolonged osmotic or nonosmotic stimulation of VP release may induce increased expression of TH immunoreactivity in the human neurosecretory neurons related to neuronal activation.

Topics: Adult; Aged; Aged, 80 and over; Cardiac Output, Low; Dehydration; Disease; Female; Humans; Hypertension, Pulmonary; Immunohistochemistry; Liver Cirrhosis; Male; Middle Aged; Neurons; Osmosis; Paraventricular Hypothalamic Nucleus; Supraoptic Nucleus; Time Factors; Tyrosine 3-Monooxygenase; Vasopressins

The first aim of this work was to investigate, under basal conditions in adult male rats, the long-term consequences of perinatal maternal food restriction on the plasma concentrations of vasopressin (VP), aldosterone and atrial natriuretic peptide (ANP) and on plasma renin activity (PRA). Furthermore, under these same conditions, the hypothalamic VP gene expression as well as the density (B(max)), affinity (K(d)) and gene expression of ANP receptors were determined in kidneys and adrenals. The second aim of this work was to examine the responsiveness to dehydration in perinatally malnourished rats. Thus, the latter parameters were studied in these rats after 72 h water deprivation.. This study was conducted on 4-Month-old male rats from mothers exposed to 50% food restriction (FR50) during the last week of gestation and lactation and on age-matched control animals (C). At this stage, both C and FR50 rats were killed by decapitation between 0900 h and 1000 h in order to determine parameters under basal conditions or after 72 h water deprivation. Plasma VP, ANP and aldosterone levels and PRA were determined by radioimmunoassay. Hypothalamic VP gene expression was determined in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) by in situ hybridization. The B(max) and K(d) values of ANP receptors were evaluated from Scatchard plots. ANP receptor gene expression was determined by Northern blot analysis.. Under basal conditions, perinatal malnutrition reduced body weight, absolute weight of kidneys and adrenals, and haematocrit. Compared with control rats, FR50 rats had significantly greater plasma VP and aldosterone levels but PRA, plasma ANP levels, plasma osmolality and hypothalamic VP gene expression were not significantly different. Perinatal malnutrition did not significantly affect glomerular ANP receptor density, but in adrenals it decreased both B(max) and K(d) values of ANP-B receptors (biological receptors) and increased B(max) of ANP-C receptors (clearance receptors). ANP-B(A) (receptor subtype A of ANP-B receptors) receptor gene expression was not significantly affected, whereas ANP-C receptor gene expression was enhanced in both adrenals and kidneys in FR50 rats. After 72 h dehydration, control rats showed a significant rise in haematocrit, plasma osmolality, PRA, circulating levels of VP and aldosterone and VP gene expression in both PVN and SON but showed a decrease in plasma ANP levels. B(max) of ANP-B receptors was decreased whereas B(max) of ANP-C receptors was enhanced in both adrenals and kidneys. ANP-B(A) receptor gene expression was not significantly affected in either kidneys or adrenals in dehydrated control rats. Similarly, ANP-C receptor gene expression was unaffected in kidneys whereas it was significantly enhanced in adrenals. In FR50 rats, the effects of water deprivation were qualitatively similar to those reported in controls concerning plasma parameters except for plasma VP levels which tended to rise (not significant) but this increase was only very slight compared with controls. Moreover, unlike controls, VP gene expression in both PVN and SON was not enhanced after dehydration in FR50 rats. In kidneys, dehydrated FR50 rats, like controls, upregulated ANP-C receptors, but they were unable to downregulate ANP-B receptors. In adrenals, unlike controls, FR50 rats enhanced ANP-B receptor density whereas they decreased both ANP-C receptor density and expression after 72 h dehydration. Similar to controls, the expression of ANP-B(A) receptors in both kidneys and adrenals as well as the expression of ANP-C receptors in kidneys, were unaffected in dehydrated FR50 rats.. Perinatal malnutrition had long-lasting effects on regulation of the fluid and electrolyte balance under basal conditions. The main effects were a significant rise in circulating levels of VP and aldosterone, and changes in density of adrenal ANP-binding sites and ANP-C receptor gene expression in both adrenals and kidneys. Perinatal malnutrition also affects the responsiveness to water deprivation with alterations in both hypothalamic VP gene expression and regulation of ANP-binding sites.

Topics: Adrenal Glands; Animal Nutritional Physiological Phenomena; Animals; Animals, Newborn; Atrial Natriuretic Factor; Binding Sites; Body Weight; Dehydration; Embryo, Mammalian; Endocrine Glands; Hormones; Hypothalamus; Kidney; Male; Nutrition Disorders; Organ Size; Rats; Rats, Wistar; Receptors, Atrial Natriuretic Factor; Tissue Distribution; Vasopressins; Water-Electrolyte Balance

The pharmacologic profile of YM471 ((Z)-4'-[4,4-difluoro-5-[2-(4-dimethylaminopiperidino)-2-oxoethylidene]-2,3,4,5-tetrahydro-1H-1-benzoazepine-1-carbonyl]-2-phenylbenzanilide monohydrochloride), a novel potent vasopressin V(1A) and V(2) receptor antagonist, was investigated using several in vitro and in vivo techniques. YM471 showed high affinity for rat vasopressin V(1A) and V(2) receptors, exhibiting K(i) values of 0.16 and 0.77 nM, respectively. In contrast, YM471 exhibited much lower affinity for rat vasopressin V(1B) and oxytocin receptors, with K(i) values of 10.5 microM and 31.0 nM, respectively. In conscious rats, oral administration of YM471 (0.1-3.0 mg/kg) produced dose-dependent inhibition of the pressor response caused by exogenous vasopressin and increased urine excretion and decreased urine osmolality; this effect lasted more than 8 h. In all biological assays used, YM471 exhibited no agonistic activity. These results demonstrate that YM471 exerts potent and long-lasting antagonistic activity on both vasopressin V(1A) and V(2) receptors, and that this compound may be a useful tool for clarifying the physiologic and pathophysiologic roles of vasopressin and the therapeutic usefulness of the vasopressin receptor antagonist.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Azepines; Decerebrate State; Dehydration; Diuresis; Diuretics; Dose-Response Relationship, Drug; Female; Furosemide; Male; Osmolar Concentration; Piperidines; Radioligand Assay; Rats; Rats, Wistar; Vasopressins

Transgenic experiments can be used to test the extent to which genes from different species can be swapped around, but still retain function, and be appropriately regulated. A vector has been developed that directs the expression of foreign genes to specific groups of vasopressin (VP) hypothalamic neurons in transgenic rats. Using this vector, we have expressed the bovine VP (bVP) RNA in the rat brain. In contrast to the situation in a mouse host, but like its endogenous rat counterpart, the mRNA encoded by the bVP transgene is subject to posttranscriptional physiological regulation in the hypothalamus; its poly(A) tail dramatically lengthens as a consequence of 3 days of dehydration. Transgene expression is also seen in the adrenal cortex, but here, despite a marked increase in transgene RNA levels with dehydration, there is no change in poly(A) tail length. These data suggest that the mouse hypothalamus and the rat adrenal gland do not have the transcript recognition or enzymatic machinery required for the physiologically responsive poly(A) tail length modulation seen in the rat brain.

Topics: Adrenal Cortex; Animals; Animals, Genetically Modified; Blotting, Northern; Cattle; Dehydration; Female; Gene Expression Regulation; In Situ Hybridization; Male; Metyrapone; Mice; Poly A; Rats; Rats, Sprague-Dawley; RNA, Messenger; Species Specificity; Tissue Distribution; Transgenes; Vasopressins

Brain-derived angiotensin II (ANG II) and prostaglandins have important roles in the regulation of body fluid and blood pressure homeostasis. In the present studies we investigated the central interactions between these two neurochemical products in regulating the hypothalamo-neurohypophysial system during dehydration. Intracerebroventricular (icv) administration of prostaglandin D(2) (PGD(2); 20 microg/5 microl) to conscious adult male Sprague-Dawley rats deprived of water for 24 h did not alter significantly the already elevated plasma levels of vasopressin or oxytocin. When PGD(2) was administered in combination with losartan, an antagonist of ANG II AT(1)-receptor subtype, however, concentrations of both hormones in plasma became further elevated. Icv administration of ANG II (50 ng/5 microl) increased further the enhanced plasma levels of vasopressin and oxytocin, as expected. Pretreatment with indomethacin (200 microg/5 microl; icv), an inhibitor of cyclo-oxygenase, significantly attenuated the ANG II-induced increase in oxytocin secretion only. Independent of the presence of ANG II, however, indomethacin decreased plasma levels of vasopressin, but not oxytocin. These results indicate that a prostaglandin is required for the stimulated release of vasopressin during dehydration and that the elevation of oxytocin secretion in response to ANG II depends largely on activation of cyclo-oxygenase and production of prostaglandins. The oxytocin response to exogenously administered PGD(2), however, can be negatively modulated by a mechanism dependent upon ANG II AT(1) receptors.

Topics: Angiotensin II; Animals; Antihypertensive Agents; Brain Chemistry; Central Nervous System; Cyclooxygenase Inhibitors; Dehydration; Indomethacin; Injections, Intraventricular; Losartan; Male; Oxytocin; Prostaglandin D2; Radioimmunoassay; Rats; Rats, Sprague-Dawley; Vasoconstrictor Agents; Vasopressins

The objective was to determine the central nervous system (CNS) responses to dehydration (c-Fos and vasopressin mRNA) in mice lacking the ANG AT(1a) receptor [ANG AT(1a) knockout (KO)]. Control and AT(1a) KO mice were dehydrated for 24 or 48 h. Baseline plasma vasopressin (VP) was not different between the groups; however, the response to dehydration was attenuated in AT(1a) KO (24 +/- 11 vs. 10.6 +/- 2.7 pg/ml). Dehydration produced similar increases in plasma osmolality and depletion of posterior pituitary VP content. Neuronal activation was observed as increases in c-Fos protein and VP mRNA. The supraoptic responses were not different between groups. In the paraventricular nucleus (PVN), c-Fos-positive neurons (57.4 +/- 10.7 vs. 98.4 +/- 7.4 c-Fos cells/PVN, control vs. AT(1a) KO) and VP mRNA levels (1.0 +/- 0.1 vs. 1.4 +/- 0.1 microCi, control vs. AT(1a) KO) were increased with greater responses in AT(1a) KO. A comparison of 1- to 2-day water deprivation showed that plasma VP, brain c-Fos, and VP mRNA returned toward control on day 2, although plasma osmolality remained high. Data demonstrate that AT(1a) KO mice show a dichotomous response to dehydration, reduced for plasma VP and enhanced for PVN c-Fos protein and VP mRNA. The results illustrate the importance of ANG AT(1a) receptors in the regulation of osmotic and endocrine balance.

Topics: Animals; Crosses, Genetic; Dehydration; Female; Gene Expression Regulation; Genes, fos; Genotype; Immunohistochemistry; In Situ Hybridization; Male; Mice; Mice, Knockout; Neurons; Pituitary Gland; Receptor, Angiotensin, Type 1; Receptors, Angiotensin; RNA, Messenger; Transcription, Genetic; Vasopressins

Aminopeptidases (APs) play a major role in the metabolism of circulating and local peptides, such as angiotensins and vasopressin, substances involved in the control of blood pressure and water balance. In the present work, we studied the influence of dehydration on angiotensinases and vasopressin-degrading activity. Since sex differences may exist in the regulation of water balance by angiotensin II and differential sexual steroid modulation of vasopressin secretion, in response to osmotic stimulation have been reported, gonadotropin releasing hormone (GnRH)-degrading activity was also analysed in serum, neurohypophysis and adrenal glands of male and female rats. Our results did not suggest sex differences in the response to changes in osmolality. GnRH-degrading activity decreased in serum of dehydrated males and females, which suggests a longer action of the peptide under these conditions. In neurohypophysis, there was an increase in the activity of aminopeptidase A (APA), the enzyme responsible for the metabolism of angiotensin II to angiotensin III. This occurs with a decrease in alanyl aminopeptidase activity, which would lead to a prolonged action of angiotensin III by reduction of its metabolism. In adrenals of dehydrated animals, the results would imply a high degree of metabolism of angiotensin III and vasopressin.

Topics: Adrenal Glands; Aminopeptidases; Animals; Dehydration; Endopeptidases; Female; Gonadotropin-Releasing Hormone; Male; Osmolar Concentration; Pituitary Gland, Posterior; Proestrus; Rats; Rats, Sprague-Dawley; Renin-Angiotensin System; Sex Factors; Vasopressins; Water Deprivation

We observed severe overhydration in an 18-month-old Japanese girl with primary polydipsia. The secretion of antidiuretic hormone (ADH) was decreased, and urinary excretion of aquaporin-2, a vasopressin-sensitive water channel protein, was suppressed under basal conditions, but the response of aquaporin-2 to ADH was essentially preserved. These findings suggest that the water channel itself was intact and that overhydration resulting from polydipsia was responsible for the decreased ADH secretion and suppression of the water channel protein.

Topics: Aquaporin 2; Aquaporin 6; Aquaporins; Child; Dehydration; Drinking Behavior; Female; Humans; Hyponatremia; Magnetic Resonance Imaging; Osmolar Concentration; Saline Solution, Hypertonic; Seizures; Vasopressins

The mammalian pineal gland is known to receive a noradrenergic innervation originating from the superior cervical ganglion which corresponds to the primary regulatory input for melatonin synthesis. However, many peptidergic fibers containing peptides such as vasopressin and oxytocin have also been found in the rat pineal gland. The present study was performed to investigate the possible role of vasopressin and oxytocin on melatonin secretion in vivo. Therefore, both neuropeptides were delivered for 2 h through a trans-pineal microdialysis probe directly into the gland at different times during the nocturnal phase of the light:dark cycle. At the same time pineal dialysates were collected continuously. Melatonin concentrations were measured by radioimmunoassay. Melatonin synthesis potentiation was achieved when vasopressin was infused locally in the pineal, during the onset of nocturnal melatonin secretion. In order to assess the possible role of a physiological increase of endogenous circulating vasopressin on pineal metabolism, melatonin synthesis was recorded in the same animals before and after a prolonged dehydration period. Night time melatonin concentration was increased after the water deprivation vs control conditions. Contrary to that, oxytocin seems not to affect pineal metabolism in the rat since no significant change was observed on melatonin secretion in response to a local oxytocin infusion. These results show that vasopressin can modulate melatonin synthesis in the rat pineal whereas no effect was obtained with oxytocin, at least under the present experimental conditions.

Topics: Animals; Circadian Rhythm; Dehydration; Drug Synergism; Infusions, Parenteral; Kinetics; Male; Melatonin; Microdialysis; Oxytocin; Pineal Gland; Rats; Rats, Wistar; Vasopressins; Water Deprivation

To determine if the aging-associated decline in testosterone results in attenuated vasopressin (VP) responses to dehydration, testosterone implants were given to aged male Fischer 344Brown-Norway F1(F344BNF1) rats. Water deprivation caused comparable dehydration, increased plasma VP (pVP), and decreased posterior pituitary (PP) VP content in 4-, 15-, and 28-month-old rats. Dehydration increased VP mRNA content of supraoptic nuclei only at 4 months, whereas VP mRNA length was increased at both 4 and 15 months of age. The elevated pVP in the water-deprived aged rats indicates that even without an increase in VP mRNA content, PP VP storage was adequate to maintain elevated pVP. Dehydration increased aquaporin-2 content at 4, but not at 15 or 28 months of age, suggesting decreased renal responsiveness to VP. Testosterone replacement did not produce dehydration-induced increases in VP mRNA or aquaporin-2. Therefore, testosterone deficiency does not result in altered VP responses to dehydration in aged F344BNF1 rats.

Topics: Aging; Analysis of Variance; Animals; Aquaporins; Blotting, Northern; Blotting, Western; Dehydration; Drug Implants; Kidney Medulla; Male; Pituitary Gland, Posterior; Progesterone; Radioimmunoassay; Rats; Rats, Inbred BN; Rats, Inbred F344; RNA; Testosterone; Vasopressins

Aquaporin 2 (AQP2), the vasopressin-regulated water channel, was originally identified in renal collecting duct principal cells. However, our recent description of AQP2 in the vas deferens indicated that this water channel may have extra-renal functions, possibly related to sperm concentration in the male reproductive tract. In this study, we have examined the regulation and membrane insertion pathway of AQP2 in the vas deferens. The amino acid sequence of vas deferens AQP2 showed 100% identity to the renal protein. AQP2 was highly expressed in the distal portion (ampulla) of the vas deferens, but not in the proximal portion nearest the epididymis. It was concentrated on the apical plasma membrane of vas deferens principal cells, and very little was detected on intracellular vesicles. Protein expression levels and cellular localization patterns were similar in normal rats and vasopressin-deficient Brattleboro homozygous rats, and were not changed after 36 h of dehydration, or after 3 days of vasopressin infusion into Brattleboro rats. AQP2 was not found in apical endosomes (labeled with Texas Red-dextran) in vas deferens principal cells, indicating that it is not rapidly recycling in this tissue. Finally, vasopressin receptors were not detectable on vas deferens epithelial cell membranes using a [(3)H]vasopressin binding assay. These data indicate that AQP2 is a constitutive apical membrane protein in the vas deferens, and that it is not vasopressin-regulated in this tissue. Thus AQP2 contains targeting information that can be interpreted in a cell-type-specific fashion in vivo.

Topics: Animals; Aquaporin 2; Aquaporin 6; Aquaporins; Base Sequence; Blotting, Western; Cell Membrane; Colchicine; Dehydration; Endosomes; Fluorescent Antibody Technique, Indirect; Immunohistochemistry; Male; Membrane Proteins; Microtubules; Rats; Rats, Brattleboro; Rats, Sprague-Dawley; Tissue Distribution; Vas Deferens; Vasopressins

The aim of our work was to study the different blood parameters as well as the activity of the vasopressinergic axis in young and mature male rats under normal conditions and following a 3-day dehydration cycle by water deprivation. Under normal conditions, our study demonstrates higher levels of vasopressin in mature rats as compared to young rats. This could be due in part to the higher blood osmolality in the mature rats. After dehydration, hypovolemia, plasmatic hyperosmolality, hypernatremia and hyperproteinemia cause a stimulation in vasopressin synthesis and release, as seen in results obtained from the hypothalamus, hypophysis and plasma in both young and mature rats. However, the response of the vasopressinergic axis to dehydration is greater in young rats, suggesting a more pronounced sensitivity to osmotic factors.

Topics: Aging; Animals; Blood Proteins; Blood Volume; Dehydration; Hematocrit; Hypernatremia; Hypothalamo-Hypophyseal System; Male; Osmolar Concentration; Potassium; Rats; Rats, Wistar; Sodium; Vasopressins

The objective of this study was to determine the effect of modulating the plasma concentrations of the avian antidiuretic hormone, arginine vasotocin (AVT), upon the febrile response to lipopolysaccharide (LPS) in Pekin ducks. LPS, intravenously administered into conscious control birds at a dose of 1 microg x kg(-1), caused a monophasic increase in body temperature of 0.85 +/- 0.12 degrees C associated with a Thermal Response Index of 2.5 +/- 0.6 C degrees h. Plasma AVT concentrations in the control birds also increased with the progression of the fever response, more than doubling from their basal values. Ducks in which the circulating level of AVT had either been elevated by the intravenous infusion of the peptide or dehydration, or reduced by the administration of a specific AVT antibody prior to LPS administration, produced body temperature profiles and Thermal Response Index values that did not differ significantly from those of the control birds. The lack of any direct effect of variations in plasma AVT concentrations upon the magnitude of the fever response indicates that the LPS-induced elevation in plasma AVT is not associated with modulating the rise in body temperature obtained in avian fever.

Topics: Animals; Arginine Vasopressin; Body Temperature Regulation; Dehydration; Ducks; Female; Fever; Lipopolysaccharides; Male; Vasopressins

Inhibiting NO synthase (NOS) with N(G)-nitro-L-arginine methyl ester (L-NAME, 250 microg/5 microl of artificial cerebrospinal fluid (aCSF)) injected intracerebroventricularly (i.c.v.) increased already enhanced levels of oxytocin, but not vasopressin, in conscious adult male Sprague-Dawley rats dehydrated for 24 h. Intracerebroventricular pretreatment with indomethacin (200 microg/5 microl aCSF), an inhibitor of cyclo-oxygenase, but not with losartan (25 microg/5 microl aCSF), an antagonist of angiotensin II (ANG II) AT(1)-receptor subtype, nearly prevented the elevation in oxytocin levels after L-NAME. Thus, NO inhibits prostaglandin (but not ANG II) mediated the modulatory actions of NO on oxytocin secretion from the hypothalamo-neurohypophysial system (HNS) during water deprivation.

Topics: Angiotensin II; Animals; Dehydration; Hypothalamo-Hypophyseal System; Indomethacin; Injections, Intraventricular; Losartan; Male; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitric Oxide Synthase; Oxytocin; Prostaglandins; Rats; Rats, Sprague-Dawley; Vasopressins; Water Deprivation; Water-Electrolyte Balance

Topics: Child; Craniopharyngioma; Craniotomy; Dehydration; Diagnosis, Differential; Female; Humans; Hypernatremia; Hypothalamic Diseases; Pituitary Neoplasms; Syndrome; Vasopressins

In the present study, we have examined in Wistar rats the effects of food or water deprivation of 3 days on the hypophyso-adrenal axis, vasopressinergic system and activity of A1 noradrenergic brain stem cell group, which is involved in the control of the hypothalamic neuro-endocrine activity. Levels of adrenocorticotropic hormone (ACTH) and vasopressin (AVP) were determined by radio-immunoassay, and corticosterone level was determined by fluorimetric method. Plasma levels of ACTH and corticosterone were greatly increased in both groups of rats. In water-deprived rats, plasma AVP (13.83 +/- 1.63 vs. 3.03 +/- 0.23 pg/ml) and osmolality levels were significantly elevated with a marked decrease of AVP hypophysis content (272 +/- 65 vs. 1098 +/- 75 ng/mg protein), but not in food-deprived rats in which osmolality did not change and AVP remained stocked (2082 +/- 216 ng/mg protein) in the hypophysis without release in the plasma (1.11 +/- 0.23 pg/ml). These observations indicated that both food-deprivation and water-deprivation stimulated the pituitary adrenal axis thereby suggesting a stress state. AVP production is stimulated both by fluid and food restriction but is secreted with differential effects: during food restriction AVP secretion is limited to supporting the hypothalamic pituitary-adrenal system.

Topics: Animals; Dehydration; Hypothalamo-Hypophyseal System; Male; Norepinephrine; Pituitary-Adrenal System; Rats; Rats, Wistar; Starvation; Vasopressins

Dehydration leads to the aggravation of gastrointestinal (GI) complaints during exercise. The aim of this study was to examine the effect of dehydration on various GI parameters during strenuous exercise. Ten healthy well-trained men were investigated in dehydrated and in euhydrated conditions. Dehydration took place before the experiments using a dehydration regimen in a sauna leading to a 3% loss of body mass. Each experiment consisted of 1 h pre-exercise rest, 1.5 h cycling at 70% maximal exercise intensity, and 3.5 h post-exercise rest. During cycling, liquid gastric emptying (GE), orocaecal transit time (OCTT) and intestinal permeability and glucose absorption were measured. The GI-symptoms were scored using a questionnaire. Body temperature, plasma volume and vasopressin were measured before and after cycling. The GE was significantly slower during dehydration [median time to peak 13C enrichment in the breath sample (13C-TTP) 23.6 min, range 13.7-50.0 min, P = 0.02] than in the control situation (median 13C-TTP 17.1 min, range 9.8-38.4 min). The OCTT was unchanged (median 173 min, range 98-263 min compared to median 128 min, range 98-195 min, P = 0.18). Dehydration did not change intestinal permeability, glucose absorption, plasma volume, rectal temperature or plasma vasopressin concentration. In the dehydration experiment, exercise induced a significant increase in nausea (P = 0.01) and epigastric cramps (P = 0.05), in contrast to the control situation. In both experiments, exercise led to a significant increase in rectal temperature and plasma vasopressin concentration, and a significant decrease in plasma volume. The increase in plasma vasopressin concentration was significantly higher in the dehydration experiment (P = 0.015). No significant differences in either the post-exercise rectal temperatures or in plasma volumes was observed. The difference in GE between the two experiments was significantly correlated with the difference in nausea score (r = 0.87, P = 0.002). We concluded that dehydration leads to a delayed GE but not to differences in OCTT, intestinal permeability or glucose uptake during intense cycling. The delay in GE is significantly associated with an increase in exercise-induced nausea.

Topics: Absorption; Adult; Bicycling; Dehydration; Digestive System; Exercise; Gastric Emptying; Gastrointestinal Diseases; Gastrointestinal Transit; Glucose; Humans; Intestinal Mucosa; Male; Osmolar Concentration; Permeability; Reference Values; Rest; Vasopressins

Angiotensin (Ang) type 1a (AT1a) receptors are critical in the control of blood pressure and water balance. Experiments were performed to determine the influence of dehydration on brain Ang receptors and plasma vasopressin (VP) in mice lacking this receptor. Control or AT1a knockout (AT1aKO) male mice were give water ad libitum or deprived of water for 48 hours. Animals were anesthetized with halothane, blood samples were collected by heart puncture, and brains were processed for Ang-receptor autoradiography with 125I-sarthran (0.4 nmol/L). Dehydration produced an increase in AT1 receptors in the paraventricular nucleus (PVN) and anterior pituitary (AP) in control mice (PVN: 70+/-16 versus 146+/-10 fmol/mg protein; AP: 41+/-7 versus 86+/-15 fmol/mg protein). No changes were noted in the median preoptic nucleus. The majority of the brain receptors were of the AT1 subtype. There was little or no specific Ang binding in AT1aKO mice and no effect of dehydration. Plasma VP levels were elevated in the halothane-anesthetized animals (>200 pg/mL) with no significant effect of dehydration. A separate experiment was performed with decapitated mice anesthetized with pentobarbital. Dehydration increased plasma VP in control mice, from 3.3+/-0.6 to 13.3+/-4.7 pg/mL, whereas no change was noted in the AT1aKO mice, 5.1+/-0.3 versus 6.1+/-0.7 pg/mL (water versus dehydration). These results demonstrate a differential response to dehydration in mice lacking AT1a receptors. There was no evidence for AT1 receptors of any subtype in the brain regions examined and no effect of dehydration on VP secretion or brain Ang receptors.

Topics: Angiotensin II; Animals; Autoradiography; Brain; Dehydration; Iodine Radioisotopes; Losartan; Male; Mice; Mice, Knockout; Paraventricular Hypothalamic Nucleus; Pituitary Gland, Anterior; Preoptic Area; Receptor, Angiotensin, Type 1; Receptors, Angiotensin; Reference Values; Vasopressins; Water Deprivation

Arginine vasopressin peptide and messenger RNA expression were examined at the cellular level in the magnocellular and parvocellular neurons in the rat paraventricular nucleus after dehydration and rehydration, employing immunocytochemistry and in situ hybridization histochemistry on the same tissue sections. Most magnocellular vasopressinergic neurons of control animals expressed both vasopressin-like immunoreactivity and messenger RNA. However, neurons negative for vasopressin-like immunoreactivity but expressing messenger RNA were also detected, and their number increased during dehydration. In contrast, almost all of the parvocellular vasopressinergic neurons of dehydrated animals expressed vasopressin messenger RNA alone, with continued increase in their number after rehydration, despite return of the number of magnocellular vasopressinergic neurons to the control level. Vasopressin messenger RNA and corticotropin releasing factor-like immunoreactivity were co-localized in the same parvocellular neurons, and vasopressin-immunoreactive nerve terminals were detected in the external zone of the median eminence. These findings suggest that magno- and parvocellular vasopressinergic neurons are differentially activated during dehydration/rehydration. Osmotic stimuli activate all magnocellular vasopressinergic neurons, but the effect is not simultaneous in all of these neurons. Parvocellular vasopressinergic neurons are also activated by the stress of dehydration which effect appears to last longer than in the magnocellular system.

Topics: Animals; Corticotropin-Releasing Hormone; Dehydration; Fluid Therapy; Gene Expression; Immunohistochemistry; In Situ Hybridization; Male; Neurons; Paraventricular Hypothalamic Nucleus; Rats; Rats, Sprague-Dawley; Reference Values; RNA, Messenger; Sodium Chloride; Tissue Distribution; Vasopressins

To test the hypothesis that subnormal thirst sensation could contribute to the development of the hypernatraemia characteristic of hyperosmolar coma, we studied osmoregulation in survivors of hyperosmolar coma.. Eight survivors of hyperosmolar coma, eight control subjects with Type II (non-insulin-dependent) diabetes mellitus and eight healthy control subjects underwent water deprivation during which measurements of thirst, plasma osmolality and vasopressin were taken.. Water deprivation caused greater peak plasma osmolality in the hyperosmolar coma group (301.7 +/- 2.7 mmol/kg) than in Type II diabetic (294.3 +/- 3.2 mmol/kg, p < 0.01) or control group (296.9 +/- 3.0 mmol/kg, p < 0.01) and a greater increase in plasma vasopressin concentration (hyperosmolar coma, 5.8 +/- 1.3 pmol/l, Type II diabetes, 1.8 +/- 1.3 pmol/l, p < 0.001, control subjects, 2.2 +/- 1.8 pmol/l, p < 0.001). Thirst ratings were lower following water deprivation in the hyperosmolar coma group (3.5 +/- 0.8 cm) than in Type II diabetes (7.7 +/- 1.6 cm, p < 0.001) or control subjects (7.4 +/- 1.3 cm, p <0.001), and the hyperosmolar group patients drank less in 30 min following water deprivation (401 +/- 105 ml) than Type II diabetic (856 +/- 218 ml, p < 0.001) or control subjects (789 +/- 213 ml, p < 0.001).. Survivors of hyperosmolar coma have subnormal osmoregulated thirst and fluid intake, which might contribute to the hypernatraemic dehydration typical of the condition.

Topics: Aged; Aged, 80 and over; Arginine Vasopressin; Blood; Dehydration; Diabetes Mellitus, Type 2; Female; Humans; Hyperglycemic Hyperosmolar Nonketotic Coma; Hypernatremia; Linear Models; Male; Middle Aged; Osmolar Concentration; Thirst; Vasopressins; Water Deprivation; Water-Electrolyte Balance

It is well known that altitude natives differ from sea level natives in aspects of fluid and electrolyte homeostasis.. To evaluate exercise and environmental influences on the electrolyte and water status in hypoxia adapted subjects, we investigated 11 well-trained marathon runners (33.7 +/- 0.7 yr, 60.5 +/- 1.9 kg), native to an altitude above 2600 m, before and after two marathon races. One competition was held at moderate altitude (AM, 2650 m, 14 degrees C, 55% RH, running time 3 h 6 min +/- 22 min) and another under tropical conditions (HM, 470 m, 28 degrees C, 70% RH, running time 2 h 54 min +/- 30 min). Blood samples were taken 3 d before, immediately after, 1 h after, and 24 h after the races.. The loss in body fluid was calculated to be 2.15 L during AM and 5.05 L during HM, respectively. It was compensated mostly by ingested fluids without electrolyte content and by metabolically produced water, which led to hyponatremia during AM (plasma [Na+] from 144.3 +/- 0.7 to 131.7 +/- 2.1 mmol x L(-1)). Severe dehydration without significant changes in plasma [Na+] could be detected after HM. Serum antidiuretic hormone concentrations and serum aldosterone concentrations significantly increased during both races and remained at a high level for at least 1h after both competitions. Serum atrial natriuretic peptide (ANP) concentrations were at a high level at rest, increasing during HM, and decreasing during AM.. Under tropical conditions, we found a severe state of dehydration characterized by an extended ANP-response, which was not prevented by water intake during the race. Under hypoxic conditions, however, we found that hyponatremia had developed. This can be partly explained by pure water intake and metabolically produced water, and also, possibly, by a special hypoxia-induced effect.

Topics: Adult; Aldosterone; Altitude; Dehydration; Electrolytes; Humans; Hypernatremia; Hypoxia; Male; Running; Vasopressins

This study examines the relationship between the threshold for plasma vasopressin concentration [PVP] responses and diuresis (Gauer-Henry reflex), and tests the hypothesis that water intake would not influence diuresis.. Eight men (19-25 yr) underwent four treatments: euhydration in air (Eu-air), euhydration in water immersion (Eu-H2O), and with prior 3.6% hypohydration in air (Hypo-air), and hypohydration in immersion (Hypo-H2O). Ad libitum drinking was allowed during the 3-h experimental and 1-h recovery periods.. Drinking was greatest during the first 10 min: 3.5 ml x kg(-1) with Hypo-air (450 ml x 3 h(-1)) and only 1.7 ml x kg(-1) (p < 0.05) with Hypo-H2O (235 ml x 3 h(-1)). At 1 h, concomitant [PVP] decreased from a control level of 6.6+/-1.5 to 4.0+/-1 .0 pg x ml(-1) (delta = 2.6 pg x ml(-1), p < 0.05) with Hypo-air, and from 5.9+/-0.6 to 2.3+/-0.2 pg x ml(-1) (delta = 3.6 pg x ml(-1), p < 0.05) with Hypo-H2O. Urine flow was unchanged from control level (<1.0 ml x min(-1)) with Hypo-air, Hypo-H2O, and Eu-air, but increased to 4-5 ml x min(-1) with Eu-H2O. Neither water intake volume nor urine flow was related to the magnitude of [PVP] depression. Regression of Uosm/Posm ratio on [PVP] and urine flow indicated that [PVP] above 2 pg x ml(-1) did not affect urine flow. Thus, ad libitum water intake in previously hypohydrated subjects did not affect urine flow or the decrease in [PVP]. The threshold [PVP] to initiate significant diuresis was about 2 pg x ml(-1), and significant diuresis can occur with no change in [PVP] maintained at about 1 pg x ml(-1) during immersion in euhydrated subjects.. Thus, it appears that the Gauer-Henry reflex is not the major mechanism for immersion-induced diuresis. Clearly, other diuretic factors are also involved.

Topics: Adult; Air; Dehydration; Diuresis; Drinking Behavior; Homeostasis; Humans; Immersion; Male; Osmolar Concentration; Reflex; Regression Analysis; Time Factors; Urodynamics; Vasopressins; Water-Electrolyte Balance

Ultrastructural studies of the supraoptic nucleus (SON) of the hypothalamus suggest that an active retraction and extension of astrocytic processes (structural plasticity) from between magnocellular neuroendocrine neurons plays a role in the release of oxytocin, vasopressin, or both peptides that accompanies parturition, lactation, and dehydration. In support of this, Salm et al. (1985) previously demonstrated a lactation-associated reduction in immunoreactive glial fibrillary acidic protein (GFAP), an astrocyte-specific cytoskeletal constituent. To determine if similar changes occur in response to dehydration, and if they are reversible, the present study examined GFAP-immunoreactivity (IR) in the SON under various hydration states. Rats were dehydrated for 7 days by substitution of drinking water with 2% saline (n = 3), or dehydrated for 7 days followed by 7 days of rehydration (n = 3). A control group (n = 3) with free access to tap water was used for comparisons. The optical density of GFAP-IR was obtained from the SON, globus pallidus, and lateral hypothalamic regions. The areas of the ventral glial limitans subjacent to the SON (SON-VGL) and of linearly equivalent segments of glial limitans more distant from the SON were also determined. Dehydration resulted in a significant reduction in GFAP-IR in the SON compared to control and rehydrated levels. We also found that the area of the SON-VGL was significantly larger than that of linearly equivalent segments of glial limitans elsewhere and that it was significantly reduced in dehydrated rats, returning to control levels with rehydration. GFAP-IR and glial limitans thickness in regions unrelated to body fluid homeostasis lateral to the SON, overlying to dorsal cortex, and subjacent to the optic chiasm were not significantly changed by hydration state. These results are similar to the changes of GFAP-IR reported for lactating rats and provide further evidence for a role of structural plasticity of astrocytes in events surrounding the selective functional activation of local neurons.

Topics: Animals; Antibodies; Astrocytes; Dehydration; Fluid Therapy; Glial Fibrillary Acidic Protein; Male; Neuronal Plasticity; Oxytocin; Rats; Rats, Inbred Strains; Supraoptic Nucleus; Vasopressins

This study determines the interaction between glutamate receptors and dehydration-induced drinking, vasopressin (AVP) release, plasma osmolality and c-fos expression in the brain of conscious rats. The NMDA receptor antagonist dizocilpine (100 nmol infused into the cerebral ventricles) suppressed drinking following either 22 h water deprivation or intragastric injection of hypertonic saline (1.5 M), attenuated the increased plasma vasopressin induced by dehydration, but had no effects on peripheral hyperosmolality caused by either water deprivation or injections of hypertonic saline. Dizocilpine had no inhibitory effects on feeding after 24 h food deprivation. Dizocilpine also suppressed c-fos expression induced by dehydration in the median preoptic nucleus (MPN), the supraoptic and paraventricular nuclei (SON and PVN), but did not influence c-fos expression in the subfornical organ (SFO). The non-NMDA receptor antagonists CNQX (400 nmol) or DNQX (60 nmol) affected neither the animals' drinking nor c-fos expression induced by dehydration. Double staining showed that suppression of c-fos expression following dizocilpine occurred in the NMDA R1 receptor containing neurons in the hypothalamus. These results suggest that the NMDA-type glutamate receptors may be involved in dehydration induced dipsogenic and neuroendocrinological responses. They complement our earlier findings that dizocilpine also attenuates drinking and c-fos expression following intraventricular infusions of angiotensin II.

Topics: Animals; Dehydration; Dizocilpine Maleate; Drinking Behavior; Excitatory Amino Acid Antagonists; Feeding Behavior; Handling, Psychological; Immunohistochemistry; Injections, Intraventricular; Male; Osmolar Concentration; Prosencephalon; Proto-Oncogene Proteins c-fos; Radioimmunoassay; Rats; Saline Solution, Hypertonic; Vasopressins

Intracerebroventricular (i.c.v.) injection of the inhibitor of NO synthase (NOS), N(G)-nitro-L-arginine methyl ester (L-NAME) (250 microg/5 microL) attenuated the drinking response in rats deprived of water for 24 h. Moreover, oxytocin (OT) levels in plasma increased after 2 min, whereas both oxytocin and vasopressin levels were elevated at 120 min after intracerebroventricular injection. The delayed effect of L-NAME on both hormones was not observed in dehydrated animals allowed to drink water. Blood pressure remained stable after injection of artificial cerebrospinal fluid (aCSF) in dehydrated rats not allowed to drink. In rats having access to water, however, there was an immediate but transient pressor response (0-5 min) with a delayed hypotension from 45 to 120 min. L-NAME consistently increased blood pressure in a biphasic mode, whether the animals drank or not, with an early peak at 5 min that decayed after 15-30 min and a second pressor response beginning at 30-45 min and remaining elevated at 120 min when the experiment ended. These pressor responses were independent of the adrenal glands. Thus, centrally produced nitric oxide facilitates drinking, inhibits release of vasopressin and oxytocin from the magnocellular system, and maintains resting arterial blood pressure in normally hydrated and dehydrated rats.

Topics: Animals; Blood Pressure; Brain; Dehydration; Drinking; Enzyme Inhibitors; Injections, Intraventricular; Male; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitric Oxide Synthase; Oxytocin; Rats; Rats, Sprague-Dawley; Vasopressins; Water Deprivation; Water-Electrolyte Balance

In order to investigate the effects of centrally administered Atrial Natriuretic Peptide (ANP) on plasma ADH and corticosterone levels as well as on blood pressure and on heart rate, 20 male New Zealand White (NZW) rabbits were used. Measurements were made on restrained conscious animals one week after the implantation of an indwelling intracerebroventricular (i.c.v.) cannula and two indwelling intravascular catheters (intracarotid and intrajugular). Animals were classified into two main groups, those with water available ad libitum ("euhydrated" group) and those who were dehydrated for 24h ("dehydrated" group) before blood pressure and heart rate recordings and blood sampling for hormonal determination. Each group's individuals were divided into two subgroups of five animals each. Blood samples were collected at 0 min (control) and 30; 60, 90, 120 min following i.c.v. administration of 25 microliters of either artificial cerebrospinal fluid (aCSF) (subgroups "aCSF") or human (h) ANP (1 microgram) in aCSF (25 microliters) (subgroups "hANP"). Blood pressure and heart rate were also recorded at the same times. Plasma ADH and corticosterone concentrations were determined by RIA. The results were analysed by ANOVA. Blood pressure and heart rate values were unaffected by water deprivation or by ANP administration. Mean plasma corticosterone levels at all times (30-120 min) were significantly higher (p < 0.001) than at 0 min time. Plasma corticosterone levels in the "dehydrated + aCSF" group were significantly higher (p < 0.05) than in each of the other groups ("dehydrated + hANP", "euhydrated + aCSF", "euhydrated + hANP"). Plasma corticosterone levels in each of those other groups did not differ significantly from one another. Dehydration resulted in an increase in ADH levels (p < 0.0001) and i.c.v. administration of hANP prevented (p < 0.05) in "dehydrated + hANP" experimental group, the increase in ADH levels observed in the control "dehydrated + aCSF" group from 90 to 120 min. The increase of corticosterone and ADH in the control dehydrated groups could possibly be due to the combined stress stimulus of dehydration and restriction in the restrain box. These results indicate that centrally administered ANP, at the concentration achieved in the present study, neither affects blood pressure and heart rate in conscious restrained euhydrated and 24h-dehydrated NZW rabbits nor decreases the ADH and corticosterone response to dehydration, but does apparently modul

Topics: Animals; Atrial Natriuretic Factor; Blood; Blood Pressure; Cerebrospinal Fluid; Corticosterone; Dehydration; Heart Rate; Injections, Intraventricular; Kinetics; Male; Osmolar Concentration; Rabbits; Vasopressins

To examine the involvement of vasopressin and dehydration in the regulation of aquaporin-2 (AQP2) expression in rat kidney, we investigated the effects of treatment for 60 h with the specific V2-receptor antagonist OPC-31260 (OPC), alone and in conjunction with dehydration for the last 12 h. Changes in AQP2 protein and mRNA expression in kidney inner medulla were determined by Western and Northern blotting, and AQP2 distribution was analyzed by immunocytochemistry and immunoelectron microscopy. Treatment with OPC increased urine output fourfold, with a reciprocal decrease in urine osmolality. AQP2 expression decreased to 52 +/- 11% of control levels (n = 12, P < 0.05), and AQP2 was found predominantly in intracellular vesicles in collecting duct principal cells. This is consistent with efficient blockade of the vasopressin-induced AQP2 delivery to the plasma membrane and with the observed increased diuresis. Consistent with this, AQP2 mRNA levels were also reduced in response to prolonged OPC treatment (30 +/- 10% of control levels, n = 9). Five days of treatment with furosemide, despite producing even greater polyuria than OPC, was not associated with downregulation of AQP2 levels, demonstrating that AQP2 downregulation is not secondary to increased urine flow rate or loss of medullary hypertonicity. During 12-h thirsting in the continued presence of OPC, urine output dropped dramatically, to levels not significantly different from that seen in (nonthirsted) control animals. In parallel with this, AQP2 levels rose to control levels. Control experiments confirmed continued effective receptor blockade. These results indicate that the V2-receptor antagonist causes a modest decrease in AQP2 expression that is not a consequence of increased urine flow rate or washout of medullary hypertonicity. However, this decrease is much less marked than that seen in some forms of acquired nephrogenic diabetes insipidus. In conjunction with the effects of thirsting, this suggests that modulation of AQP2 expression is mediated partly, but not exclusively, via V2 receptors.

Topics: Animals; Aquaporin 2; Aquaporin 6; Aquaporins; Benzazepines; Dehydration; Diuresis; Diuretics; Furosemide; Gene Expression; Immunohistochemistry; Ion Channels; Kidney Medulla; Male; Microscopy, Immunoelectron; Polyuria; Rats; Rats, Wistar; RNA, Messenger; Vasopressins; Water Deprivation

Despite the known potent vasoconstrictor effects of vasopressin, the role of this hormone in the maintenance of blood pressure is incompletely understood. In studies performed in animals with increased plasma vasopressin concentrations, several complex cardiovascular effects have been noted, including decreases in heart rate and cardiac output, which may account for a lack of effect on arterial pressure despite the vasopressin-induced increase in total peripheral resistance. Only a few studies have been done to assess the cardiovascular effects of vasopressin in human subjects, and most of these have been limited to measurement of heart rate and arterial pressure only. The present study was designed to identify more fully the cardiovascular effects of vasopressin when plasma vasopressin concentrations are increased by osmotic stimulation without the superimposition of major nonosmotic stimuli associated with severe volume depletion.. Studies were performed on 11 normal human subjects in supine and erect posture before and after 24 hours of fluid deprivation, and following administration of a selective V1 receptor antagonist, [d(CH2)5Tyr(ME)]AVP, after dehydration. Cardiovascular parameters were measured noninvasively by thoracic electrical bioimpedance cardiography and blood samples for measurements of plasma concentrations of vasopressin and other hormones affected by dehydration and differences in posture were collected for subsequent analysis.. After 24 hours of fluid restriction, plasma osmolality was increased from 287 +/- 0.9 to 294 +/- 0.7 mosm/kg H20 and plasma vasopressin concentrations (Pavp) were increased in both supine and erect posture. Mean arterial (MAP) and systolic blood pressure (SBP) were reduced by fluid restriction but were higher in erect than in supine posture both before and after fluid restriction. Heart rate (HR), diastolic blood pressure (DBP), and systemic vascular resistance (SVRI) were also higher in erect than in supine posture, while cardiac index (CI), stroke index (SI), end-diastolic index (EDI), and an index of total thoracic fluid content (TFC) were all reduced in erect posture, both before and after dehydration. Plasma renin activity (PRA) and plasma norepinephrine concentrations (Pne) were increased in erect posture, both before and after dehydration, but there was no effect of erect posture on plasma vasopressin concentrations (Pavp), either before or after dehydration. Administration of the V1 receptor antagonist after dehydration had no effect on hemodynamic parameters other than small reductions in DBP and cardiac preload.. It is concluded from these studies that small increases in Pavp associated with moderate dehydration do not play a role in the maintenance of arterial pressure in normal human subjects in either supine or erect posture.

Topics: Adult; Aged; Antidiuretic Hormone Receptor Antagonists; Arginine Vasopressin; Dehydration; Female; Hemodynamics; Hormone Antagonists; Humans; Male; Middle Aged; Posture; Vasoconstrictor Agents; Vasopressins

Topics: Aging; Animals; Aquaporin 2; Aquaporin 6; Aquaporins; Dehydration; Drug Implants; Gene Expression Regulation, Developmental; Hematocrit; Kidney Medulla; Male; Pituitary Gland, Posterior; Rats; Rats, Inbred F344; Supraoptic Nucleus; Testosterone; Vasopressins

N-Methyl-D-aspartate receptors are thought to be involved in synaptic signaling within the hypothalamo-neurohypophysial system, but the extent and nature of their involvement has not been determined. In this study, in the rat, we evaluated the effect of hyperosmotic stimulation on the N-methyl-D-aspartate receptor subunit, NR1, which confers function to N-methyl-D-aspartate receptor heteromers. Co-localization of immunoreactivity for NR1 and vasopressin- or oxytocin-associated neurophysin in magnocellular neurons of the supraoptic and paraventricular hypothalamic nuclei was accomplished using double-label immunohistochemistry. Our results show that vasopressin- and oxytocin-neurophysin-positive populations contained detectable levels of NR1 labeling. Using NR1 labeling as a measure of N-methyl-D-aspartate receptor density, we examined the effect of dehydration in these nuclei. Using computer-assisted densitometry, we found significantly greater NR1 labeling densities in the magnocellular regions of both the supraoptic and paraventricular nuclei of saline-treated rats than of control rats. This increase was not due to methodological factors, since no changes in NR1 labeling density were found in a nearby nucleus, the nucleus reuniens. Western blot analysis showed similar selective increases in NR1 labeling in homogenates from the supraoptic nucleus, paraventricular nucleus and in some cases from the anterior hypothalamic area. In both immunohistochemical and western blotting experiments we did not observe a dehydration-induced increase in NR1 in other brain areas examined. Our results showing an up-regulation of NR1-containing N-methyl-D-aspartate receptors during dehydration suggest that these receptors are involved in the regulation of body water and may represent an adaptive physiological response following activation of the hypothalamo-neurohypophysial axis. In addition, these results suggest that the functional expression of N-methyl-D-aspartate receptors is dynamic and may be modified according to the physiological state of the animal.

Topics: Animals; Blotting, Western; Dehydration; Immunohistochemistry; In Vitro Techniques; Male; Neuronal Plasticity; Neurophysins; Oxytocin; Paraventricular Hypothalamic Nucleus; Rats; Receptors, N-Methyl-D-Aspartate; Supraoptic Nucleus; Up-Regulation; Vasopressins; Water-Electrolyte Balance

The relative contribution of cellular and extracellular water deficits to the genesis of thirst due to thermal dehydration was studied in male Sprague-Dawley rats following exposure to a 40 degrees C environment for 4 h. Intragastric (I.G.) and intravenous (I.V.) preloads of water reduced the elevated plasma sodium and plasma osmolality of thermally dehydrated rats to control levels, but preloads of saline did not. I.G. and I.V. preloads of saline returned the hematocrit and plasma protein concentration of thermally dehydrated rats to control levels. Both the I.G. water preload and the I.G. saline preload reduced water intake, with the I.G. water preload having a greater effect. The I.V. water preload reduced water intake nearly to control levels, whereas the I.V. saline preload was without effect on water intake. These data indicate that the water intake of thermally dehydrated rats is primarily due to a cellular water deficit and that oral and gastric factors are also important in terminating water intake in thermally dehydrated rats.

Topics: Animals; Atrial Natriuretic Factor; Body Temperature Regulation; Dehydration; Drinking; Homeostasis; Hot Temperature; Male; Rats; Rats, Sprague-Dawley; Thirst; Vasopressins; Water Loss, Insensible; Water-Electrolyte Balance

Our goal was to study the water balance in healthy breast-fed infants (n = 139) during their first 5 days, by cross-sectional measurements of body weight, serum sodium, serum osmolality, and hematocrit. We also investigated infants' capacity to conserve body water by increased secretion of vasopressin, the main antidiuretic hormone in human beings.. The maximal body weight reduction was 5.7% +/- 1.7% (mean +/- SD) of birth weight and most infants started to gain weight when they were 3 days old. The serum sodium level at 16 +/- 4 hours (on day of birth) was 142 mmol/L; the level increased after 1 day (p < 0.01) and remained constantly high for the following 2 days (p < 0.05). The serum osmolality was increased at 1 day (p < 0.01) and 2 days (p < 0.05) compared with the value on the day of birth (296 mOsm/kg). The plasma vasopressin level was constant up to 24 hours (1 day), but decreased during the next 2 days (p < 0.01). Infants with body weight reduction exceeding 10% (n = 15) had a further elevation of the serum sodium level (p < 0.0001) and serum osmolality (p < 0.0001), and the plasma vasopressin level was twofold higher (p < 0.0001) compared with corresponding levels in infants with less weight reduction. These infants also had a reduced interval between two subsequent feedings (p < 0.001). The hematocrit remained unchanged irrespective of the degree of weight reduction.. When the reduction of body weight exceeds 10%, the newborn infant releases vasopressin in response to fluid hypertonicity. This state also affects feeding behavior, perhaps as an expression of thirst. It is likely that hormone release is also stimulated in parallel with a weight reduction of less than 10%, because it is also accompanied by a hyperosmotic state.

Topics: Body Weight; Cross-Sectional Studies; Dehydration; Female; Hematocrit; Humans; Infant, Newborn; Male; Osmolar Concentration; Plasma; Sodium; Thirst; Vasopressins; Water-Electrolyte Balance; Weight Loss

The effect of different rates of fluid ingestion on heart rate, rectal temperature, plasma electrolytes, hormones and performance was examined during prolonged strenuous exercise conducted at 21 degrees C. Seven well-trained males (24 +/- 1 yr; 68.6 +/- 2.9 kg; VO2 peak = 4.69 +/- 0.17 L min-1; mean +/- SEM) cycled for 2 h at 69 +/- 1% VO2 peak while receiving either no fluid replacement (NF), a volume of water estimated to prevent body weight loss (FR-100 = 2.32 +/- 0.10 L 2 h-1) or 50% of this volume (FR-60 = 1.16 +/- 0.05 L 2 h-1). The 2-h exercise bout was followed by a ride to exhaustion at a workload estimated to be 90% VO2 peak. After 2 h of exercise, NF was associated with a 3.2 +/- 0.1% weight loss, while FR-50 and FR-100 resulted in losses of 1.8 +/- 0.1 and 0.1 +/- 0.1%, respectively. Compared with FR-100, heart rate and rectal temperature were elevated (P < 0.05) during the second hour of exercise in NF, with FR-50 intermediate. Reductions in plasma volume during exercise were greater in NF and FR-50, compared with FR-100 and plasma sodium concentration was elevated in NF, decreased slightly in FR-100, with FR-50 intermediate. Plasma renin activity, aldosterone and atrial natriuretic peptide increased to similar extents in the three trials. Plasma vasopressin remained unchanged for FR-100, increased for NF, with intermediate values for FR-50. Exercise time to exhaustion at 90% VO2-peak was longer in FR-100 (328 +/- 93 s) than NF (171 +/- 75 s) with FR-50 (248 +/- 107 s) not significantly different from either FR-100 or NF. In conclusion, the responses of heart rate, rectal temperature, plasma sodium, and vasopressin during, and performance following, prolonged cycling exercise conducted at 21 degrees C are related to the amount of fluid ingested (i.e. the degree of dehydration).

Topics: Adult; Aldosterone; Atrial Natriuretic Factor; Body Temperature; Dehydration; Drinking; Exercise; Heart Rate; Humans; Male; Potassium; Renin; Sodium; Vasopressins

The ability of the kidney to regulate water balance is impaired with age, although the secretion of vasopressin is maintained in senescent animals. This suggests that the cellular response to antidiuretic hormone is reduced in aging kidney. To test this hypothesis, the relationship between the expression of the vasopressin. V2 receptor mRNA and adenosine 3',5'-cyclic monophosphate (cAMP) accumulation was investigated in the medullary thick ascending limb of Henle's loop (MTAL) of adult and aging rats. Tubular suspensions of MTAL were prepared from 10- and 30-mo-old female WAG/Rij rats. The accumulation of cAMP for maximal concentration of vasopressin was 34% larger in adult than in old animals (9.5 +/- 0.5 pmol/4 min, n = 16, and 7.1 +/- 0.6 pmol/4 min, n = 12, respectively). The concentration of vasopressin corresponding to half-maximal stimulation was similar in the two groups (0.66 +/- 0.20 and 0.52 +/- 0.09 nmol, n = 5, in adult and old animals), indicating comparable sensitivity of the renal cells with age. The age-related impaired response to vasopressin of the V2 receptor was specific for females and was not observed in males. Direct stimulation of adenylyl cyclase by forskolin induced a comparable accumulation of cAMP in adult and senescent rats. The V2 receptor mRNA level in the MTAL was constant between 10 and 30 mo whether the animals were normally hydrated or dehydrated for 2 days. These data indicate that, in MTAL, the age-related impaired cAMP accumulation by vasopressin would be linked to a change either in the translation of V2 mRNA or in posttranslational processing mechanisms or in the coupling between the V2 receptor and adenylyl cyclase.

Topics: 1-Methyl-3-isobutylxanthine; Aging; Angiotensin II; Animals; Chick Embryo; Cyclic AMP; Dehydration; Dose-Response Relationship, Drug; Female; Hydrolysis; Loop of Henle; Osmolar Concentration; Phosphodiesterase Inhibitors; Rats; Rats, Inbred Strains; Receptors, Vasopressin; RNA, Messenger; Vasopressins

The plasma vasopressin (VP) response to 72 h of water deprivation is attenuated in 30-mo-old Fischer 344 (F344) rats relative to 4-mo-old rats. This appears to reflect an inability to increase VP synthesis. In contrast, elevated plasma VP has been reported in the Brown-Norway (BN) strain of rats secondary to reduced renal VP responsivity. The response to dehydration in the F1 cross of these strains (F344BNF1) was evaluated. Male rats, 4 and 30 mo old, were deprived of water for 72 h or allowed water ad libitum. In response to dehydration, plasma sodium and hematocrit were significantly increased in both young and aged rats (P < 0.05), but plasma VP, urine osmolality, and aquaporin 2 expression were only increased in the young rats (P < 0.05). Posterior pituitary content of immunoreactive VP was depleted in the young but not the old rats. Thus the aged F344BNF1 rats demonstrated a deficit in VP release in response to an apparently similar dehydration stimulus. This deficit was different from those previously reported for either the F344 or BN strains. Thus further studies are required to determine the abnormalities underlying this response.

Topics: Aging; Analysis of Variance; Animals; Aquaporin 2; Aquaporin 6; Aquaporins; Crosses, Genetic; Dehydration; Hematocrit; Ion Channels; Kidney Medulla; Male; Pituitary Gland, Posterior; Rats; Rats, Inbred BN; Rats, Inbred F344; Sodium; Urine; Vasopressins

Exercise increases plasma arginine-vasopressin (PAVP), plasma atrial natriuretic peptide (PANP), plasma renin activity (PRA), and plasma aldosterone (PALDO) in an intensity-dependent manner. With acute exercise, urine osmolality (UOSM) is often decreased despite increased PAVP. The hyperbaric environment lowers PAVP and UOSM, and increases urine flow.. If work produced similar renal effects at hyperbaria, greater than normal dehydration could result from larger free water losses.. To test this hypothesis, hormonal and renal responses were assessed during exercise at 80% of maximum heart rate at 46 atmospheres absolute (atm abs) in 3 males, and during maximum exercise at 37 atm abs in 4 males.. This maximum exercise was performed at the highest pressure thus far reported and revealed no loss in peak power output. Maximum O2 consumption and heart rate were only slightly reduced, 9.5% and 7% respectively, despite a 41% reduction in maximum minute ventilation. Basal levels and the changes resulting from maximum exercise in PRA and PALDO were unaffected by pressure, but basal and exercise-stimulated levels of PANP and PAVP were reduced compared with 1.5 atm abs control values. UOSM was not significantly affected during maximal exercise at sea level, but during maximum exercise at 37 atm abs and submaximum exercise at 46 atm abs UOSM increased over 300 mosm.kg-1 and 180 mosm.kg-1, respectively.. Contrary to the hypothesis, UOSM was increased by about 200 mosm.kg-1 by both exercise protocols during hyperbaric exposure and free water was conserved.

Topics: Adult; Aldosterone; Arginine; Atmospheric Pressure; Atrial Natriuretic Factor; Dehydration; Diving; Exercise; Heart Rate; Humans; Kidney; Male; Osmolar Concentration; Oxygen Consumption; Renin; Urine; Vasopressins

The existence of efferent connections between tuberomammillary (TM) and the supraoptic (SON) nuclei led us to study the morphological changes at these levels during dehydration induced in rats by repeated administration of hypertonic saline. The dehydration effects are evaluated by three parameters: nucleus area, argyrophilic nucleolar organizer regions (Ag-NOR) area, and mean number of Ag-NORs. These parameters reflect the level of transcriptional activity of the rRNA genes, which in turn is closely related to the protein synthesis activity of the cell. The technique used is argyrophilic staining which labels the nucleolar organizer regions (NORs) of the nucleoli in the neurons and their area, permitting their quantification with an image analysis system. The statistical analysis reflects the sensitivity to dehydration of these structures at TM level. Our results support the regulatory role of vasopressin secretion by SON through the histaminergic pathways arising from TM in rat dehydration processes.

Topics: Animals; Dehydration; DNA, Ribosomal; Gene Expression Regulation; Histamine; Male; Mammillary Bodies; Nucleolus Organizer Region; Rats; Rats, Wistar; RNA, Ribosomal; Silver Staining; Sodium Chloride; Supraoptic Nucleus; Transcription, Genetic; Tuber Cinereum; Vasopressins

Topics: Animals; Biological Transport; Dehydration; Hypothalamus; Immunohistochemistry; Male; Oxytocin; Peptides; Pituitary Gland; Rats; Rats, Wistar; Vasopressins

Water intake following dehydration was studied in pregnant (N = 5), lactating (N = 4) and nonpregnant, nonlactating (N = 5) Swedish domestic goats (Capra hircus) to investigate if reproductive period affected drinking. Plasma cortisol concentration and the hematocrit value were measured to evaluate stress. The goats were water deprived from 9.00 h until 15.05 h the next day. They were fed at 7.00 and 15.20 h. On the second day, ambient temperature was increased from 20 degrees C to 38-39.5 degrees C for 5.15 h to accelerate water losses. Water temperature during rehydration was 35 +/- 1 degree C. Plasma Na concentration and osmolality increased most in dehydrated and heat-stressed pregnant and lactating goats. Pregnant goats lost 2.2 kg of their body weight. They drank 3.5 l immediately, followed by 2.5 l during afternoon eating. Lactating goats lost 4.9 kg and drank 6.3 l at once, and 3.9 l during feeding. Nonpregnant, nonlactating goats lost 1.7 kg and drank 2.6 l followed by 0.6 l. The large water consumption in pregnant and lactating goats caused hyponatremia and hemodilution, but they continued to drink during the night (0.5 +/- 0.2 l and 0.8 +/- 0.5 l, respectively). Renal free water clearance increased in all periods, with a long-lasting water diuresis during pregnancy. Plasma cortisol concentrations and the hematocrit values rose in connection with water intake. These results imply that the thirst center became less sensitive to inhibitory signals from the oropharyngeal tract and the diluted blood plasma during pregnancy and lactation. Catching sight of water was the most exciting procedure during these experiments.

Topics: Animals; Blood Proteins; Body Temperature; Body Weight; Dehydration; Drinking; Female; Goats; Hematocrit; Hot Temperature; Hydrocortisone; Lactation; Pregnancy; Reproduction; Respiration; Sodium; Urination; Vasopressins

Regulation of total body water balance in amphibians by antidiuretic hormone (ADH) contributed to their successful colonization of terrestrial habitats approximately 200-300 million years ago. In the mammalian kidney, ADH modulates epithelial cell apical membrane water permeability (Pf) by fusion and retrieval of cytoplasmic vesicles containing water channel proteins called aquaporins (AQPs). To determine the role of AQPs in ADH-elicited Pf in amphibians, we have identified and characterized a unique AQP from Bufo marinus called AQP toad bladder (AQP-TB). AQP-TB possesses many structural features common to other AQPs, AQP-TB is expressed abundantly in ADH-responsive tissues, including toad urinary bladder and skin as well as lung, skeletal muscle, kidney, and brain. In a manner identical to that reported for the mammalian ADH-elicited water channel AQP2, AQP-TB expression is increased significantly by intervals of dehydration or chronic ADH stimulation. However, expression of AQP-TB protein in Xenopus laevis oocytes does not significantly increase oocyte Pf. The lack of expression of functional AQP-TB water channels in oocytes may result from intracellular sequestration of AQP-TB due to the presence of a YXRF sequence motif present in its carboxyterminal domain.

Topics: Amino Acid Sequence; Animals; Base Sequence; Blotting, Northern; Bufo marinus; Cell Membrane Permeability; Cloning, Molecular; Dehydration; DNA, Complementary; Endosomes; Epithelial Cells; Epithelium; Flow Cytometry; Immunoblotting; Ion Channels; Molecular Sequence Data; Oocytes; Sequence Homology; Tissue Distribution; Urinary Bladder; Vasopressins; Water

Our previous demonstration of sexual dimorphism in the antidiuretic response to exogenous vasopressin prompted us to investigate the response to moderately high levels of endogenous vasopressin stimulated by water deprivation in conscious rats. After 24 h water deprivation, urine flow was significantly higher and urine osmolality lower in females than in males. Plasma concentrations of vasopressin were higher in females than in males after water deprivation, but plasma osmolality did not differ. Gonadectomy, which had no effect in dehydrated males, decreased urine flow and increased urine osmolality in females to levels observed in intact and gonadectomized males. Spontaneous water intake was also measured and found to be lower in males and estrous females than in females in the other phases of the estrous cycle. These observations support the concept that there is a gender difference in the antidiuretic responsiveness to endogenous vasopressin, that this difference is dependent upon the ovarian hormones, and that it may lead to differences in consumptive behavior.

Topics: Animals; Dehydration; Female; Kidney Concentrating Ability; Male; Rats; Rats, Sprague-Dawley; Sex Factors; Vasopressins

Hyponatremia following subarachnoid hemorrhage (SAH) occurs due to the inappropriate secretion of antidiuretic hormone (SIADH). However, this condition is also sometimes associated with certain dehydration states.. To clarify the pathogenesis, daily values of urine volume, water balance, and sodium balance (Na Bal) were correlated with plasma levels of atrial natriuretic peptide (ANP), antidiuretic hormone (ADH), and plasma renin activity (PRA) in 31 cases of SAH.. Na Bal was markedly negative on days 2 and 3. Cumulative Na Bal showed continuous negative values until day 10 following SAH. ANP values showed a consistent elevation, while ADH showed only an initial surge. PRA, as the gross indicator of circulatory volume, showed a lack of suppression, indicating no increase in the circulatory volume.. Hyponatremia following SAH therefore appears to be the result of increased natriuresis, due to the inappropriate elevation of ANP rather than SIADH. In this situation, water restriction should not be recommended, since the circulatory volume is decreased.

Topics: Adult; Aged; Aneurysm, Ruptured; Atrial Natriuretic Factor; Body Water; Dehydration; Female; Humans; Hyponatremia; Intracranial Aneurysm; Male; Middle Aged; Natriuresis; Renin; Subarachnoid Hemorrhage; Vasopressins

The effects of osmotic stimulation on Fos expression and cell size increase in the supraoptic nucleus were evaluated in intact, sham-operated, and AV3V-lesioned rats. Fos-positive neurons were found mainly in the AV3V regions and the hypothalamic magnocellular neurons in the forebrain in dehydrated intact rats. Intraperitoneal injection of hypertonic saline and chronic dehydration induced a significant increase in number of Fos-positive neurons in the supraoptic nucleus of intact and sham-operated rats. AV3V lesions completely abolished the expression of Fos in SON neurons of rats that were intraperitoneally injected with hypertonic saline and were chronically dehydrated. Chronic dehydration increased significantly cell size of the OXT and AVP magnocelluar neurons in intact and sham-operated rats. However, there was no increase in cell size of those in the AV3V-lesioned rats. These results demonstrate that neural input derived from AV3V regions plays a significant role in causing Fos expression and structural changes such as cell size increase in the hypothalamic magnocellular neurons with osmotic stimulation.

Topics: Animals; Cell Size; Cerebral Ventricles; Dehydration; Gene Expression; Hypothalamus; Immunohistochemistry; Male; Neurons; Oncogene Proteins v-fos; Oxytocin; Rats; Rats, Wistar; Vasopressins

The regulation of mRNA for aldose reductase, sorbitol dehydrogenase, and the Na+/Cl-/taurine cotransporter was studied with three in vivo models in which urinary concentration is reduced: Sprague-Dawley rats undergoing a water diuresis or fed a low-protein diet or Brattleboro rats. In Sprague-Dawley rats, 3 days of water diuresis reduced inner medullary aldose reductase mRNA abundance 6.5-fold compared with untreated rats, whereas sorbitol dehydrogenase and taurine cotransporter mRNA were unchanged. When water diuretic rats were acutely deprived of water, urine osmolality increased significantly after 4 h but aldose reductase mRNA did not increase until 12 h. Heat shock protein-70 mRNA was not increased by water deprivation. Second, in rats fed a low-protein diet for 3 wk, aldose reductase mRNA increased two-fold, whereas sorbitol dehydrogenase and taurine cotransporter mRNA were unchanged. Finally, in Brattleboro rats, urine osmolality and levels of aldose reductase and taurine cotransporter mRNA increased in response to 1 day of water deprivation, whereas sorbitol dehydrogenase mRNA was unchanged. Administering vasopressin (1 U/day) to Brattleboro rats for 8 days also increased urine osmolality and aldose reductase mRNA but did not alter sorbitol dehydrogenase or taurine cotransporter mRNA. This result is consistent with the hypothesis that changes in urine osmolality induce changes in aldose reductase mRNA abundance that are independent of vasopressin. It was concluded that, in rat inner medulla: (1) aldose reductase mRNA abundance varies with changes in water balance or dietary protein, whereas sorbitol dehydrogenase and taurine cotransporter mRNA do not; and (2) heat shock protein-70 mRNA abundance is not increased during acute osmotic stress.

Topics: Aldehyde Reductase; Animals; Blotting, Northern; Carrier Proteins; Dehydration; Diet, Protein-Restricted; Diuresis; Heat-Shock Proteins; Kidney Medulla; L-Iditol 2-Dehydrogenase; Male; Membrane Glycoproteins; Membrane Transport Proteins; Osmolar Concentration; Rats; Rats, Brattleboro; Rats, Sprague-Dawley; RNA, Messenger; Specific Pathogen-Free Organisms; Taurine; Vasopressins

We investigated the expression of pituitary adenylate cyclase-activating polypeptide (PACAP) mRNA in rat brain by in situ hybridization. PACAP mRNA was prominently expressed in arcuate nucleus (ARC). Three days of water deprivation significantly increased plasma arginine vasopressin and markedly potentiated the expression of PACAP mRNA in ARC. These results suggest that PACAP in ARC may play some physiological role, possibly one of which may be the control of vasopressin release.

Topics: Animals; Arcuate Nucleus of Hypothalamus; Autoradiography; Dehydration; In Situ Hybridization; Male; Neuropeptides; Neurotransmitter Agents; Pituitary Adenylate Cyclase-Activating Polypeptide; Rats; RNA, Messenger; Vasopressins

Sheep which were predominantly urinary excretors (U) or faecal excretors (F) of sodium were exposed to a 75% reduction of water intake for 72 h. The experiment was performed on moderate, low or high sodium intakes (0.4, 0.05 or 1.2 mmol kg-1 day-1) to test the hypothesis that dehydration natriuresis was not a cause of sodium depletion but a defence against hypernatraemia. Dehydration caused elevation of plasma sodium concentration, osmolality, antidiuretic hormone (ADH) and oxytocin but, as in other experiments, a fall in haematocrit. The two higher levels of sodium intake were associated with dehydration natriuresis but also a smaller increase in faecal sodium excretion in both U and F sheep. On low sodium intake, however, neither urinary nor faecal sodium excretion increased in either group of sheep although the rise in plasma sodium concentration caused by dehydration was similar. Thus, when there is a risk of sodium depletion, due to low sodium intake, dehydration natriuresis does not occur, consistent with the hypothesis. Active sodium transport inhibitor (ASTI) and atrial natriuretic peptide (ANP) fell rather than rose during dehydration. Since aldosterone is suppressed by the higher levels of sodium intake, none of these hormones is likely to mediate dehydration natriuresis in sheep. F sheep showed more effective renal and faecal water conservation when dehydrated. During water restriction, the urinary potassium excretion of U sheep was significantly reduced, unlike that of F sheep; moreover, the latter maintained an identical plasma potassium concentration between baseline and restriction period, whereas in U sheep it was 0.3 mmol l-1 higher during water restriction. Increased drinking rather than reduced urine output was the basis of rehydration when ad lib. water intake was restored.

Topics: Animals; Atrial Natriuretic Factor; Dehydration; Feces; Female; Natriuresis; Oxytocin; Sheep; Sodium; Sodium Chloride, Dietary; Vasopressins; Water; Water Deprivation

Experiments were carried out on 9- to 11-week-old male and female Sprague-Dawley rats. Dot-blot analysis and 3'-end digoxigenin-labeled 26mer oligonucleotide probe were used in the investigation of vasopressin (AVP) mRNA level in the hypothalamus of male and female rats. The normal hypothalamic AVP-mRNA level in males was 48% higher than that in females (P < 0.05). Plasma osmolality was also higher in males than in females (P < 0.05). In dehydrated rats, the hypothalamic AVP-mRNA level was 2.47 and 1.98 times in females (P < 0.001) and males (P < 0.01), respectively, as much as in their normal controls; the difference in hypothalamic AVP-mRNA level between dehydrated females and males was statistically insignificant. Plasma osmolality was higher in dehydrated females than in dehydrated males (P < 0.01). In salt-loaded rats, hypothalamic AVP-mRNA level was 2.47 and 2.17 times in females (P < 0.001) and males (P < 0.01), respectively, as much as in their controls. The difference in hypothalamic AVP-mRNA level between salt-loaded males and females was not statistically significant. Plasma osmolality in salt-loaded females was also higher than that in salt-loaded males (P < 0.001). These findings indicate that there is sex difference in hypothalamic AVP mRNA level and plasma osmolality under normal conditions; during dehydration and salt-loading AVP mRNA level increases and the difference in AVP mRNA level between males and females becomes insignificant.

Topics: Animals; Base Sequence; Dehydration; Female; Hypothalamus; Male; Molecular Sequence Data; Osmolar Concentration; Rats; Rats, Sprague-Dawley; RNA, Messenger; Sex Factors; Sodium Chloride, Dietary; Vasopressins

The purpose was to determine whether extracellular volume or osmolality was the major contributing factor for reduction of thirst in air and head-out water immersion in hypohydrated subjects. Eight males (19-25 yr) were subjected to thermoneutral immersion and thermoneutral air under two hydration conditions without further drinking: euhydration in water (Eu-H2O) and euhydration in air, and hypohydration in water (Hypo-H2O) and hypohydration in air (3.7% wt loss after exercise in heat). The increased thirst sensation with Hypo-H2O decreased (P < 0.05) within 10 min of immersion and continued thereafter. Mean plasma osmolality (288 +/- 1 mosmol/kgH2O) and sodium (140 +/- 1 meq/l) remained elevated, and plasma volume increased by 4.2 +/- 1.0% (P < 0.05) throughout Hypo-H2O. A sustained increase (P < 0.05) in stroke volume accompanied the prompt and sustained decrease in plasma renin activity and sustained increase (P < 0.05) in plasma atrial natriuretic peptide during Eu-H2O and Hypo-H2O. Plasma vasopressin decreased from 5.3 +/- 0.7 to 2.9 +/- 0.5 pg/ml (P < 0.05) during Hypo-H2O but was unchanged in Eu-H2O. These findings suggest a sustained stimulation of the atrial baroreceptors and reduction of a dipsogenic stimulus without major alterations of extracellular osmolality in Hypo-H2O. Thus it appears that vascular volume-induced stimuli of cardiopulmonary baroreceptors play a more important role than extracellular osmolality in reducing thirst sensations during immersion in hypohydrated subjects.

Topics: Adult; Air; Atrial Natriuretic Factor; Body Water; Central Nervous System; Dehydration; Extracellular Space; Head; Humans; Immersion; Male; Osmolar Concentration; Plasma Volume; Pressoreceptors; Renin; Sensation; Stroke Volume; Thirst; Vasopressins; Water

To investigate the origin of posterior pituitary high intensity (PPHI) seen on T1-weighted magnetic resonance (MR) images.. Six rabbits, including four rabbits deprived of drinking water for 4 days and two control rabbits, were examined by MR imaging. Plasma vasopressin levels were sequentially measured by radioimmunoassay. Pituitary glands were immunostained with guinea pig anti-rabbit vasopressin antibody, and ultrathin sections of Epon/Araldite-embedded specimens were observed with a transmission electron microscope.. In control rabbits, PPHI was noted on T1-weighted MR images, and the posterior pituitary lobe was positively immunostained with anti-vasopressin antibody. At the ultrastructural level, nerve terminals contained numerous neurosecretory granules bearing vasopressin. Conversely, plasma vasopressin levels gradually increased and PPHI was absent in 4-day dehydrated rabbits. The posterior lobe was scarcely stained with anti-vasopressin antibody, and neurosecretory granules were rarely observed. However, a number of small dispersed vesicles, possibly derived from the fragmentation of neurosecretory granule envelopes, were seen in the nerve terminal.. Posterior pituitary high signal seen on T1-weighted MR images is attributed to neurosecretory granules bearing vasopressin.

Topics: Animals; Cytoplasmic Granules; Dehydration; Epoxy Resins; Image Enhancement; Immunohistochemistry; Magnetic Resonance Imaging; Male; Microscopy, Electron; Nerve Endings; Neurosecretion; Phthalic Anhydrides; Pituitary Gland, Posterior; Plastic Embedding; Rabbits; Radioimmunoassay; Vasopressins

Brain cytoplasmic 1 (BC1) RNA is a small non-translated RNA polymerase III transcript. Because this RNA can be detected in the rat posterior pituitary with 35S in situ hybridization autoradiography, it has been hypothesized that this RNA might be transported in the axons of hypothalamo-neurohypophyseal neurons. In the present study, we aimed to determine the cellular localization of BC1 more precisely by using non-radioactive in situ hybridization of BC1 RNA at both the light and electron microscopic levels. Our studies revealed that BC1 RNA was indeed located intra-axonally. Furthermore, BC1 RNA was abundant within a subset of axonal swellings and/or terminals, and was also found in discrete cytoplasmic domains of undilated axonal segments. Using a semiquantitative in situ hybridization approach, we have measured and compared the changes in BC1 RNA and arginine vasopressin (AVP) mRNA during dehydration (chronic salt-loading) and rehydration. Chronic salt-loading significantly increased both BC1 RNA and AVP mRNA. The increase in BC1 RNA labelling (2.5-fold), however, was modest and somewhat less enduring than the increase in AVP mRNA labelling (13-fold). Upon rehydration, both the BC1 and vasopressin transcripts in the posterior pituitary rapidly returned to control values. In conclusion, like vasopressin mRNA, BC1 RNA is transported in axons of the hypothalamo-neurohypophyseal system where it aggregates in a subset of axonal swellings, and its axonal transport is similarly regulated. Therefore, we propose that BC1 RNA might be involved in the axonal targeting, docking and/or transport of AVP or other axonal mRNAs.

Topics: Animals; Blotting, Northern; Brain; Dehydration; Fluid Therapy; In Situ Hybridization; Male; Pituitary Gland, Posterior; Rats; Rats, Sprague-Dawley; RNA, Messenger; Vasopressins

I.c.v. administration of a nitric oxide (NO) synthase inhibitor (NG-monomethyl-L-arginine, NMMA, 500 micrograms/5 microliters) to conscious rats deprived of water for 24 h attenuated drinking and decreased glucose utilization in the subfornical organ and median preoptic nucleus. NMMA did not alter the enhanced glucose utilization in the hypothalamo-neurohypophysial system (HNS) of dehydrated rats, although it has been shown to increase, selectively, oxytocin (OT) secretion [18]. This suggests that NO may act in the neural lobe to inhibit OT secretion and promote the preferential release of vasopressin during dehydration. This effect is similar to the blockade of endogenous opiate receptors by naloxone.

Topics: Amino Acid Oxidoreductases; Animals; Arginine; Dehydration; Deoxyglucose; Drinking; Glucose; Hypothalamo-Hypophyseal System; Injections, Intraventricular; Male; Nitric Oxide Synthase; omega-N-Methylarginine; Oxytocin; Preoptic Area; Rats; Rats, Sprague-Dawley; Subfornical Organ; Vasopressins

The present study was performed to evaluate the role of central vasopressin in cardiovascular regulation. First, a novel vasopressin V1 antagonist (OPC21268) was injected intracerebroventricularly in conscious rats. In water-deprived animals, the mean arterial blood pressure (MABP) and heart rate were significantly decreased compared with euhydrated control rats. There was, however, no significant difference in the concentration of vasopressin in the perfusate of cerebrospinal fluid between groups. Second, vasopressin was intracerebroventricularly injected in male and female homozygous Brattleboro rats. The increase in MABP was greater in males than in females. These results suggest that central vasopressin is involved in blood pressure regulation in pathophysiological states.

Topics: Animals; Blood Pressure; Cardiovascular Physiological Phenomena; Cardiovascular System; Dehydration; Female; Heart Rate; Injections, Intraventricular; Male; Piperidines; Quinolones; Rats; Rats, Brattleboro; Sex Factors; Vasopressins

Dehydration induces Fos expression and increases the length of the vasopressin (VP) mRNA poly-A tail and the content of VP mRNA in the supraoptic (SON) and paraventricular nuclei (PVN) of the hypothalamus. The current studies were performed to evaluate the effect of aging on these responses. Fischer 344 rats of 4, 14, and 28-30 months of age were either water deprived for 72 h or allowed ad libitum access to water. Fos induction in the SON and PVN was examined by immunocytochemistry in order to provide an index of cellular activation. VP mRNA content and size was examined in SON by Northern analysis as an index of VP synthetic capacity. Dehydration induced the expected increase in plasma osmolality in all three ages, however, serum VP was only increased in the 4- and 14-month-old rats. The increase in serum VP was accompanied by a decrease in VP content of the posterior pituitary (PP) in the dehydrated 4- and 14-month-old rats. PP VP content was reduced in both the hydrated and dehydrated old rats relative to the other ages (P = 0.0007). Fos was induced in both SON and PVN of all water deprived rats regardless of age. The density of Fos staining was increased in both nuclei following dehydration (SON, P = 0.002; PVN, P = 0.0001). There was also a significant increase in the number of cells expressing Fos in both nuclei in the dehydrated animals (SON, P = 0.002; PVN, P = 0.0056). There was no significant effect of age on the density of Fos staining. In contrast, dehydration failed to elicit the expected increase in VP mRNA size and content in the SON of the aged dehydrated rats although both of these parameters were increased in the 4- and 14-month-old rats (P < 0.05). Thus, the inability of old Fischer rats to increase serum VP during chronic dehydration is not caused by decreased activation of the neurons (as indicated by Fos induction), but apparently reflects depletion of PP stores of VP due to an inability to increase the amount of VP mRNA available for translation.

Topics: Aging; Animals; Blotting, Northern; Dehydration; Gene Expression; Genes, fos; Image Processing, Computer-Assisted; Immunohistochemistry; Male; Paraventricular Hypothalamic Nucleus; Rats; Rats, Inbred F344; RNA, Messenger; Supraoptic Nucleus; Vasopressins

1. In many mammals, severe dehydration is known to cause exhaustion of the vasopressin content of the neural lobe. Here, we have examined the physiological state of the neurohypophysis of the jerboa Jaculus orientalis, a rodent inhabitant of a semi-desert climate. 2. Isolated neurohypophyses and neurosecretory nerve endings were perfused in vitro and vasopressin and oxytocin release were determined by radioimmunoassay. 3. Electrical stimulation of the neurohypophysis with bursts of pulses mimicking the activity of hypersecreting neuroendocrine neurones induced similar increases of secretion in both control animals and animals dehydrated for up to 2 months. Neurohormone release was greatly potentiated when the bursts of pulses were separated by silent intervals. 4. Prolonged stimulation of neurohypophyses from both control and dehydrated animals induced a sustained increase of vasopressin release; in contrast, oxytocin release under similar conditions showed a biphasic secretory pattern consisting of a transient increase that subsequently decreased to a steady level whose amplitude was similar to that for vasopressin. 5. K(+)-induced secretion was largely inhibited by the Ca2+ channel blockers nicardipine and omega-conotoxin, suggesting that in this neurosecretory system both L- and N-type calcium channels play a major role in stimulus-secretion coupling. Depolarization of isolated nerve endings using a fast-flow perifusion system showed that there was no difference in the amplitude and the time course of the secretory response in dehydrated and hydrated animals. 6. The results demonstrate that, despite the climatic conditions in which the jerboas live, their neural lobes retain the capacity to release, upon depolarization of the plasma membrane of the nerve endings, large amounts of neurohormone. It is concluded that the neurohypophyseal peptidergic release system in the dehydrated jerboa functions adequately even under extreme environmental stress.

Topics: Animals; Calcium Channel Blockers; Calcium Channels; Cell Membrane; Dehydration; Electric Stimulation; Nerve Endings; Oxytocin; Perfusion; Pituitary Gland, Posterior; Potassium; Radioimmunoassay; Rodentia; Vasopressins

We have previously shown that prolonged alcohol ingestion leads to neuronal loss in the supraoptic nucleus of the rat and that the surviving neurons, mainly the vasopressinergic ones, display marked increase in volume. In an attempt to establish correlates for the volumetric alterations we have studied the organelles of supraoptic nucleus neurons in three groups of rats--ethanol-fed, pair-fed, and dehydrated, in all cases treated from 2 to 12 months of age. The volume and surface area of the rough endoplasmic reticulum and Golgi apparatus, and the volume of nucleoli and neurosecretory granules were estimated on the basis of the respective volume and surface densities. The volumes and surface areas of all quantified organelles were increased in both alcohol-fed and dehydrated animals, although the increases were greater in the former group. Changes in the organelles studied are commonly regarded as reliable indicators of the neurosecretory activity of magnocellular neurons. Thus, our results suggest that under conditions of chronic alcohol exposure, the synthesizing activity of the surviving supra-optic neurons is augmented to compensate for the alcohol-induced neuronal loss and/or as a consequence of the alcohol-induced hyperosmolality. Changes in the transport and release of the neurosecretory material cannot, however, be ruled out as an additional cause of neuronal enlargement.

Topics: Adaptation, Physiological; Alcoholism; Animals; Cell Size; Dehydration; Ethanol; Male; Neurons; Organelles; Osmolar Concentration; Rats; Rats, Wistar; Stereotaxic Techniques; Supraoptic Nucleus; Vasopressins; Water-Electrolyte Balance

Renal Na excretion during the 24 h following feeding was studied in sheep. A pronounced natriuresis occurred 3.5-5.5 h after feeding. Na excretion then fell to low levels in animals allowed to drink water, but was significantly elevated above this level in water-deprived sheep for most of the remaining period. Both the post-prandial and dehydration-induced natriuresis were prevented by intracerebroventricular (icv) infusions of low Na concentration 0.3 mol l-1 mannitol at 1 ml h-1, and a water diuresis also occurred. These effects were not caused by icv infusion of artificial cerebrospinal fluid (Na concentration = 150 mmol l-1). As a result, there was a much greater increase in plasma Na concentration and osmolality in the sheep given icv mannitol. Intravenous infusion of vasopressin prevented the water diuresis induced by icv mannitol, but the inhibition of natriuresis was still observed and plasma Na concentration increased by 8 mmol l-1 over 24 h compared with an increase of 3 mmol l-1 in dehydrated sheep infused icv with artificial cerebrospinal fluid. The results show that the ambient Na concentration in the brain plays an important role in the normal homeostatic regulation of Na balance by the kidney in sheep.

Topics: Animals; Brain; Captopril; Cerebrospinal Fluid; Dehydration; Eating; Female; Injections, Intraventricular; Natriuresis; Osmolar Concentration; Reference Values; Sheep; Sodium; Vasopressins; Water Deprivation

Secretion of the antidiuretic hormone (ADH) vasopressin is increased when body fluid homeostasis is disturbed by dehydration. Associated with this increased secretion is an elevation of vasopressin mRNA in magnocellular hypothalamic neurons projecting to the posterior pituitary. The proto-oncogene c-fos codes for a nuclear phospho-protein Fos which binds to specific DNA elements and acts as a transcriptional regulator coupling short-term extracellular stimuli to long-term responses by altering secondary target gene expression. This study in rats examined the time courses of dehydration induced c-fos expression and the change of vasopressin gene expression in the magnocellular neurons of the hypothalamus. Immunocytochemical and in situ hybridization study demonstrated that c-fos was induced by acute intracellular dehydration in the hypothalamic magnocellular nuclei of paraventricular (PVN), supraoptic (SON), and accessory groups such as nucleus circularis. Double-label immunocytochemical study co-localized Fos and vasopressin-neurophysin immunoreactivity in the same magnocellular neurons in the SON and PVN. In situ hybridization analysis after acute dehydration revealed a rapid and transient c-fos induction followed by a persistent increase in vasopressin mRNA for up to 2 days even after rehydration. Furthermore, prevention of c-fos translation by pretreatment with protein synthesis inhibitor cycloheximide attenuated this dehydration induced increase in vasopressin mRNA. This study demonstrated that an increase in vasopressin transcription after acute dehydration is dependent on an early phase of protein synthesis.

Topics: Animals; Arginine Vasopressin; Dehydration; Gene Expression Regulation; Genes, fos; Hypothalamus; Male; Nerve Tissue Proteins; Neurophysins; Osmolar Concentration; Rats; Rats, Sprague-Dawley; Saline Solution, Hypertonic; Structure-Activity Relationship; Vasopressins

Intracerebroventricular (i.c.v.) administration of NG-monomethyl-L-arginine monoacetate (NMMA; 500 micrograms; 402 mM) and NG-nitro-L-arginine methyl ester (NAME; 270 micrograms; 200 mM), inhibitors of nitric oxide synthase, enhanced the rise in oxytocin but not vasopressin levels in plasma of conscious rats following 24 h of water deprivation. This effect of NMMA occurred by 10 min after administration, reached its peak at 15 min and decreased by 20 min. Daily administration of lower doses (50 micrograms and 0.5 microgram/5 microliter, i.c.v.) of another inhibitor of nitric oxide synthase, NG-nitro-L-arginine, just before and after 24 h of water deprivation and in control animals treated similarly were without effect on either vasopressin or oxytocin levels. Nitric oxide, therefore, attenuates preferentially the release of oxytocin during dehydration.

Topics: Amino Acid Oxidoreductases; Animals; Arginine; Dehydration; Male; Nerve Tissue Proteins; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitric Oxide Synthase; omega-N-Methylarginine; Oxytocin; Paraventricular Hypothalamic Nucleus; Pituitary Gland, Posterior; Rats; Rats, Sprague-Dawley; Supraoptic Nucleus; Vasopressins

Rats euhydrated and dehydrated during two or four days were given intracerebroventricularly (i.c.v.) thyrotropin-releasing hormone (TRH) in a daily dose of 200 ng dissolved in 10 microliters of 0.9% sodium chloride. A single dose of TRH injected to euhydrated animals increased the hypothalamic vasopressin content but did not affect significantly the content of vasopressin in the neurohypophysis as well as that of oxytocin both in the hypothalamus and neurohypophysis. In rats deprived of water for two days TRH completely prevented the decrease of neurohypophysial oxytocin due to stimulation of osmoreceptor origin. Similarly, TRH restrained both the hypothalamic and the neurohypophysial vasopressin and oxytocin depletion in rats dehydrated for four days.

Topics: Animals; Dehydration; Hypothalamo-Hypophyseal System; Hypothalamus; Male; Oxytocin; Pituitary Gland, Posterior; Radioimmunoassay; Rats; Rats, Wistar; Thyrotropin-Releasing Hormone; Vasopressins

Ethanol ingestion affects the hypothalamo-neurohypophysial system resulting in increased diuresis, dehydration and hyperosmolality. We studied the supraoptic nucleus, of the hypothalamus, in ethanol-treated rats, to determine if ethanol alone and/or the associated disturbances of water metabolism lead to structural alterations in a nucleus known to play a central role in fluid homeostasis. Groups of male and female rats were ethanol-treated until 12 and 18 months of age and compared with age-matched pair-fed controls. Twelve and 18-month-old control groups and 12-month-old water control groups (rats submitted to chronic dehydration) were also included in this study in an attempt to differentiate between the effects of undernutrition and dehydration/hyperosmolality, and the specific neurotoxic effects of ethanol. We estimated the volume of the supraoptic nucleus and the numerical density of its neurons and calculated the total number of supraoptic neurons. The volume of both supraoptic neurons and neuropil were also estimated. In immunostained material the ratio of vasopressin to oxytocin neurons and the cross-sectional areas of the two neuronal types were evaluated. There was marked neuronal loss in alcohol-treated rats, but the volume of the supraoptic nucleus was increased. The increase in the volume of the supraoptic nucleus correlated with and was due to increases in the volume was particularly marked for vasopressin neurons. No significant differences were found between controls and pair-fed controls in any of the parameters investigated. In water control rats, the volume of the supraoptic nucleus and of the supraoptic neurons and neuropil was also greater than in pair-fed controls. However, the variations found were not as marked as in ethanol-treated rats and there was no cell loss. These findings reveal, for the first time, that chronic ethanol consumption affects the morphology of supraoptic neurons and neuropil and, consequently, the structure of the entire supraoptic nucleus. Moreover, this study supports the view that ethanol has direct neurotoxic effects on supraoptic neurons because the alterations that occur are not mimicked in animals in which water metabolism alone is disturbed.

Topics: Animals; Brain; Dehydration; Ethanol; Female; Immunohistochemistry; Male; Neurons; Organ Size; Oxytocin; Rats; Rats, Wistar; Sex Characteristics; Supraoptic Nucleus; Vasopressins; Water-Electrolyte Balance; Weight Gain

A 70-year-old woman was admitted because of disturbance of her consciousness. Physical examinations and laboratory data suggested hypothyroidism. Primary hypothyroidism was subsequently confirmed with endocrinological examinations. Antidiuretic hormone (ADH) levels were elevated despite severe hyponatremia. On admission, urinary sodium concentration was 10mEq/l. The patient was treated with saline intravenously; serum sodium level increased from 120 to 125mEq/l and urinary sodium concentration increased from 10 to 54mEq/l. Mental confusion developed and serum sodium level dropped with urinary sodium concentration above 20mEq/l when thyroid replacement was started with the cessation of saline infusion. The patient's state of consciousness, elevated ADH levels, decreased serum sodium level and urinary sodium concentration were improved by thyroid replacement together with hydrocortisone therapy. Effects of acute water loading were abnormal with the administration of iodothyronine (T3) alone but were normalized with the administration of hydrocortisone together with T3. On discharge she was treated with the oral administration of levothyroxine alone. Pituitary hormones were normal. These results suggest that the patient was in a state of hypoadrenocorticism. Impaired water excretion in a state of hypoadrenocorticism due to hypothyroidism may give rise to an inappropriate secretion of ADH thereby resulting in hyponatremia, which in turn leads to hypotonic dehydration induced by water intoxication.

Topics: Adrenal Cortex; Adrenal Insufficiency; Aged; Dehydration; Female; Humans; Hyponatremia; Hypothyroidism; Vasopressins; Water Intoxication

Studies to assess the relationship between plasma arginine vasopressin concentration (Pavp) and plasma osmolality (Posm) were performed on an elderly patient with dementia who developed severe hypernatremia due to inadequate water intake following a debilitating hip fracture. Serum sodium concentrations were 174 and 196 mEq/L on two consecutive hospital admissions. During the second of these admissions, sequential measurements of Pavp and Posm were obtained as hypernatremia was gradually corrected. Pavp during this period was correlated with Posm (r = 0.887, P < 0.01), but was low despite the presence of hyperosmolality and volume depletion. Pavp decreased from 0.56 microU/mL to 0.18 microU/mL as Posm decreased from 396 to 338 mOsm/kg H2O. The regression line of this relationship intercepted the abscissa at 320 mOsm/kg H2O. Hypertonic sodium chloride infusion to reassess this relationship 2 days following the correction of hypernatremia increased Pavp only to 0.67 microU/mL while increasing Posm from 297 to 316 mOsm/kg H2O. Nevertheless, Pavp and Posm were significantly correlated (r = 0.937, P < 0.001). The slope of the regression line was 0.031, and Posm at the abscissal intercept was 292 mOsm/kg H2O. A similar increase in Posm from 290 to 310 mOsm/kg H2O during hypertonic sodium chloride infusion 11 days following the correction of hypernatremia increased Pavp to 1.95 microU/mL (r = 0.786, P < 0.05). The magnitude of the increase in Pavp at this time was equivalent to that previously observed in studies of normal subjects. The slope (0.048) and abscissal intercept (280 mOsm/kg H2O) of linear regression were also consistent with observations in studies of normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aged; Aged, 80 and over; Dehydration; Humans; Hypernatremia; Male; Regression Analysis; Vasopressins; Water-Electrolyte Balance

A study was performed investigating the daily patterns of hormone release accompanying changes in fluid balance in the male rat during 48 h of dehydration. The blood volume decreased by 18%, the largest change occurring during the initial period when the rats showed an effective loss of body sodium. During the second day of dehydration, sodium retention was again seen. Plasma sodium concentrations showed a progressive increase, the total rise being 5-6%; the greatest changes were seen during the dark phases of the cycle which may be due to the nocturnal food intake. Plasma vasopressin and oxytocin concentrations were significantly elevated throughout dehydration to levels which could be reproduced by acutely increasing plasma sodium and decreasing blood volume to the same extent. The observed increases were influenced by the phase of the day-night cycle, being greatest over the dark phases of the cycle. The overall increases were greatest when dehydration commenced at the start of the dark phase. Dehydration initially led to a rise in plasma corticosterone concentrations, whilst plasma concentrations of atrial natriuretic peptide were decreased. Plasma angiotensin II concentrations rose significantly during the later period of sodium retention.

Topics: Angiotensin II; Animals; Atrial Natriuretic Factor; Blood Volume; Circadian Rhythm; Corticosterone; Dehydration; Male; Oxytocin; Photoperiod; Pituitary Gland, Posterior; Pituitary Hormones, Posterior; Radioimmunoassay; Rats; Rats, Sprague-Dawley; Sodium; Vasopressins

Topics: Animals; Chronic Disease; Dehydration; Female; Immunohistochemistry; Nerve Endings; Oxytocin; Pituitary Gland, Posterior; Rats; Vasopressins

Rats euhydrated and dehydrated for two or four days were given intracerebroventricularly (i.c.v.) thyrotropin-releasing hormone (TRH) in a daily dose of 200 ng dissolved in 10 microliters of 0.9% sodium chloride.) A single dose of TRH administered to euhydrated animals was followed by a significant increase of the vasopressin content in the neurohypophysis and hypothalamus as well as of the hypothalamic oxytocin content. On the contrary, a single dose of TRH decreased the oxytocin content in the neurohypophysis. Under conditions of dehydration TRH distinctly restrained the decrease of vasopressin and oxytocin in the hypothalamus. In animals dehydrated for two or four days the decrease of oxytocin in the neurohypophysis, brought about by stimulation of osmoreceptors, was distinctly more marked under treatment with TRH. On the contrary, the depletion of neurohypophysial vasopressin was significantly less apparent under such conditions. 28 nmol/L TRH markedly increased vasopressin release but inhibited that of oxytocin from the neurointermediate lobes incubated in vitro both under basal conditions as well as during stimulation with excess (56 mmol) potassium.

Topics: Animals; Dehydration; Hypothalamus; In Vitro Techniques; Injections, Intraventricular; Male; Oxytocin; Pituitary Gland, Posterior; Potassium; Rats; Rats, Wistar; Thyrotropin-Releasing Hormone; Vasopressins

Topics: Animals; Biopterins; Body Water; Dehydration; Hypothalamus; Male; Oxytocin; Pituitary Gland, Posterior; Rats; Rats, Wistar; Reference Values; Vasopressins

1. The vasopressin mRNA in the adult male rat hypothalamus is modulated in two distinct ways by a dehydration stimulus. In addition to the well-established increase in transcript abundance, it has recently been demonstrated that the vasopressin mRNA poly(A) tail increases in length. 2. We have studied the ontogeny of poly(A) tail length modulation in neonates in response to milk deprivation and found that poly(A) tail length changes are age dependent. In neonates older than 12 days of age, the vasopressin mRNA poly(A) tail length increased with milk deprivation and this effect became more marked in older animals. However, in rats 5 to 9 days old, milk deprivation resulted in a detectable though not significant decrease in vasopressin mRNA poly(A) tail length. 3. As milk deprivation is a combination of dehydration and starvation, we investigated the effect of the latter stimulus in more mature animals. We found that starvation modifies the length of the vasopressin mRNA poly(A) tail in a manner opposite that due to dehydration. 4. Our data indicate a novel mode of regulation of the vasopressin mRNA, namely, poly(A) tail shortening. This system provides a model for future studies concerning the adaptive role of poly(A) tail length modulation in response to physiological stimuli.

Topics: Adaptation, Physiological; Age Factors; Animals; Animals, Newborn; Dehydration; Female; Hypothalamus; Male; Osmolar Concentration; Poly A; Rats; Rats, Sprague-Dawley; RNA, Messenger; Starvation; Vasopressins; Weight Loss

The effect of CCK-8 (50 ng, i.c.v.) on the neurohypophysial vasopressin and oxytocin storage was estimated in haemorrhaged (1 ml per 100 g b.w.) male Wistar rats. In another experimental series rats dehydrated for three days were given CCK-8 in a daily i.c.v. dose of 50 ng. The neurohypophysial vasopressin and oxytocin content was bioassayed by pressor effect following Dekański or milk-ejection activity in vitro following van Dongen and Hays, respectively. The decrease of neurohypophysial vasopressin and oxytocin content, brought about by dehydration, was significantly less marked in animals treated with CCK-8. The depletion of neurohypophysial vasopressin and oxytocin content in haemorrhaged animals could be completely inhibited by earlier i.c.v. administration of CCK-8. It is suggested that hypothalamic cholecystokinin may serve as a modulator of neurohypophysial function.

Topics: Animals; Bloodletting; Dehydration; Disease Models, Animal; Hemorrhage; Injections, Intraventricular; Male; Models, Biological; Oxytocin; Pituitary Gland, Posterior; Rats; Rats, Wistar; Sincalide; Vasopressins

Experiments were performed to test a possible role of (6R)-5,6,7,8-tetrahydro-alpha-biopterin dihydrochloride (BH4) in the neurohypophysial vasopressin and oxytocin content in euhydrated and dehydrated rats. Chronic treatment with BH4, administered to not dehydrated animals, was followed by a significant decrease of neurohypophysial vasopressin, but not of neurohypophysial oxytocin. In dehydrated animals the neurohypophysial vasopressin content decreased progressively; this process was not affected significantly by BH4. In rats dehydrated and treated simultaneously with BH4 the decrease of neurohypophysial oxytocin content was distinctly less marked.

Topics: Animals; Biopterins; Dehydration; Male; Oxytocin; Pituitary Gland, Posterior; Rats; Rats, Wistar; Vasopressins

Effects of dehydration on vasopressin-secreting cells (VP cells) of the supraoptic nucleus (SON) and the paraventricular nucleus (PVN) in the Mongolian gerbils were studied immunocytochemically and morphometrically. The plasma osmolality was measured at the time of sacrifice of individual animals and the body weight was measured every day during dehydration. The plasma osmolality increased significantly on day 3 of dehydration, followed by a gradual increase to reach nearly its equibilium state on day 10. The body weight decreased rapidly until day 10, followed by a gradual decrease thereafter. The area of VP cells increased significantly in both the SON and PVN on day 1 of dehydration, the level being nearly the same until days 3 to 5 and going up on day 7 to reach the plateau after day 15. These findings seem to reflect a compensation mechanism between the volume of body fluid and the plasma osmolality and to reflect responses of VP cells to the osmotic stimuli. Electron microscopic observation revealed that, at the beginning and late stages of dehydration, the increase in the area of VP cells was in parallel with the expansion of the Golgi area and with the distension of cisternae of the rough endoplasmic reticulum.

Topics: Animals; Body Weight; Dehydration; Gerbillinae; Immunohistochemistry; Male; Microscopy, Electron; Osmolar Concentration; Paraventricular Hypothalamic Nucleus; Rodent Diseases; Supraoptic Nucleus; Vasopressins

Intracerebroventricular hANP (50 nmol) inhibits release of vasopressin and oxytocin following dehydration as well as after haemorrhage. 10 nmol/L hANP markedly inhibits vasopressin and oxytocin release in vitro from the neurointermediate lobes both under basal condition as well as during stimulation with excess (56 mM) potassium. It is suggested that ANP may serve as a modulator of vasopressin and oxytocin release. The respective processes are localized, at least in part, at the neurohypophysial level.

Topics: Animals; Atrial Natriuretic Factor; Dehydration; Femoral Vein; Hemorrhage; Injections, Intraventricular; Male; Oxytocin; Pituitary Gland, Posterior; Pituitary Hormones, Posterior; Potassium; Rats; Rats, Wistar; Vasopressins

Plasma concentrations of prolactin were measured in male sheep (wethers, n = 8) during 120 min exposure to mild physical stress (restraint), and also following I.V. injection of 30 micrograms ovine corticotrophin-releasing factor (CRF), when the animals were water replete and when they had been deprived of water for 48 h. Restraint stress produced a small increase in prolactin secretion (n.s.) when the animals were euhydrated and a large increase (P less than 0.001) when they were dehydrated. Administration of CRF had no effect on prolactin concentrations in either experimental condition. In a further study in which euhydrated animals (n = 6) were subjected to restraint while receiving infusions of vasopressin (1 microgram/h), there was no enhancement of basal or stress-induced prolactin secretion. Thus, dehydration enhances stress-induced prolactin release in sheep through a process that does not involve a pituitary action of CRF or circulating vasopressin.

Topics: Animals; Corticotropin-Releasing Hormone; Dehydration; Male; Prolactin; Restraint, Physical; Sheep; Stress, Physiological; Vasopressins

It has been shown that during physiological stimuli, such as dehydration, supraoptic nucleus (SON) neurons undergo profound morphological changes. However, little is known about how much each type of cell, oxytocin (OT) or vasopressin (VP), contributes to this plasticity during dehydration. Using postembedding immunogold cytochemistry for both OT and VP hormones at the electron microscopic level, we address this question. Rats were chronically dehydrated (given 2% saline to drink for 10 days) and their SON neurons were studied morphologically. The results were compared to control animals with free access to water. Both VP and OT somata showed an enlargement in size in dehydrated animals. Percentage of somasomatic/dendritic membrane contact increased significantly in both VP and OT neurons, with no significant changes in percentage of coverage of the cells by astrocytic membrane. Only the VP cells had a lesser amount of axosomatic membrane contact after dehydration, possibly due to an increase in cell size rather than a decrease in synaptic contact. Multiple synapses (MSs) (i.e., terminals that form more than one synapse with adjacent somata and or dendrites) occurred only between positively labeled cells and between negatively labeled cells, but not between positively and negatively labeled cells. The number of MSs per 100 microns OT somatic membrane or per 100 OT cells was significantly higher in dehydrated rats but was unchanged with regard to VP neurons. These findings indicate that both VP and OT neurons undergo morphological changes during chronic dehydration and, thus, that plasticity is not limited to OT cells as some earlier reports have suggested.

Topics: Animals; Dehydration; Female; Immunohistochemistry; Male; Microscopy, Electron; Neuronal Plasticity; Oxytocin; Rats; Supraoptic Nucleus; Vasopressins

The addition of cobalt chloride to the female rat blood serum resulted in a decrease of serum osmolality and in an increase of ionized calcium concentration probably due to ousting of calcium out of proteins and alteration of proteins characteristics. The osmolality of saline and activities of sodium, potassium and calcium in it did not change following addition of Co2+. The administration of vasopressin and dehydration were not followed by alteration of characteristics of serum reaction in response to addition of Co2+ in rats. More obvious effect of Co2+ was revealed with high initial serum osmolality.

Topics: Animals; Calcium; Cobalt; Dehydration; Female; Ions; Male; Osmolar Concentration; Potassium; Rats; Rats, Inbred Strains; Sodium; Vasopressins

Endogenous arginine vasopressin was previously shown to modulate the rate of loss of functional (CNS) tolerance to ethanol, suggesting that chronic ethanol ingestion might alter vasopressin synthesis and/or release. Since extrahypothalamic vasopressin is believed to be involved in the CNS effects of the peptide, we determined the effect of ethanol on vasopressin mRNA in the bed nucleus of the stria terminalis (BST), as well as in several hypothalamic nuclei. Chronic ethanol ingestion, that produced functional tolerance and physical dependence in mice, resulted in decreased vasopressin mRNA levels in all areas examined. In contrast, as expected, dehydration resulted in increases in vasopressin mRNA in the BST and in all hypothalamic nuclei except the suprachiasmatic nucleus. In the BST, both ethanol ingestion and dehydration affected cells in the central region of the nucleus, while cells in the caudal portion were only affected by ethanol treatment. The results indicate that chronic ethanol ingestion generally reduces the synthesis of vasopressin, and that increased vasopressin synthesis is not necessary in order for the peptide to affect ethanol tolerance.

Topics: Animals; Brain Chemistry; Dehydration; Drug Tolerance; Ethanol; Hypothalamus; Male; Mice; Mice, Inbred C57BL; Neurons; Nucleic Acid Hybridization; RNA, Messenger; Supraoptic Nucleus; Vasopressins

Two experiments were carried out using adult castrated sheep prepared with jugular vein catheters. In Experiment 1, sheep (N = 8) were injected iv with saline vehicle, vehicle + 15 or 30 micrograms oCRH, or subjected to 120 min mild physical stress (restraint), following a 48 h period during which water was freely available or withheld. Blood samples were taken for 30 min before and 120 min after oCRH injection, and before and during restraint, and the plasma analysed for AVP and cortisol content. Levels of AVP increased by over 500% after dehydration, but were unaffected by oCRH or restraint. In contrast, plasma cortisol was unchanged after dehydration, but increased after oCRH and restraint. Moreover, these cortisol responses were significantly greater when the sheep were dehydrated. In Experiment 2, euhydrated sheep (N = 6) were infused iv with saline vehicle or vehicle + AVP for a 5-h pretreatment period, followed by a 2-h experimental period in which the animals were injected with 15 micrograms oCRH or subjected to 120 min restraint, as in Experiment 1. Blood samples were taken throughout the experiment from a contralateral catheter and the plasma analysed for AVP and cortisol content. The AVP infusion produced plasma levels of the hormone approximately twice those seen after 48 h dehydration in Experiment 1, but did not affect cortisol secretion. Furthermore, the cortisol response to oCRH, or restraint, was not enhanced by the AVP infusion. These results suggest that pituitary responsiveness to exogenous or endogenous CRH (restraint stress) may be enhanced in sheep by dehydration through a mechanism that does not involve an adrenal or pituitary action of circulating AVP.

Topics: Adrenal Cortex; Animals; Corticotropin-Releasing Hormone; Dehydration; Hydrocortisone; Immobilization; Injections, Intravenous; Radioimmunoassay; Sheep; Time Factors; Vasopressins

In the course of aging, the renal concentrating ability is markedly reduced. This defect may result from an inappropriate synthesis of antidiuretic hormone in the central nervous system or may be due to an impaired renal response to vasopressin. The two hypotheses have been studied in vivo in rats and in vitro in mice. The results of these studies indicated that: 1) dehydration induces a comparable release of vasopressin along the hypothalamo-hypophysial axis in 10, 20 and 30 month-old rats; 2) there is no change with age of the number of nephrons, single nephron filtration rate or transport capacity of Henle's loop of cortical nephrons which could account for an impaired renal response to vasopressin; 3) the reduced concentrating ability of the kidney appears to be linked to a decreased response of the medullary thick ascending limb of Henle's loop which in part is responsible for the cortico-papillary gradient of solutes within the kidney.

Topics: Age Factors; Aging; Animals; Dehydration; Female; In Vitro Techniques; Kidney; Loop of Henle; Mice; Osmolar Concentration; Pituitary Gland; Rats; Rats, Inbred Strains; Vasopressins

The influence of mild dehydration on plasma levels of atrial natriuretic peptide (ANP) was studied in both young (aged 18 to 25 years) and elderly (aged 72 to 86 years) subjects. We expected that dehydration would lower ANP concentrations due to the ensuing volume contraction. A different response of the ANP hormonal system in the elderly might help to explain the observation that elderly subjects are more predisposed to dehydration as compared to young subjects. Dehydration was induced by restriction of fluid intake to 25% of normal for one day. During the study, urinary osmolality increased while osmolar clearance and body weight decreased. Basal ANP concentrations were higher in the elderly subjects. However, these levels did not change during the dehydration study neither in the young nor in the elderly subjects. This may be explained by the activation of counter-regulatory systems preventing a decrease in central blood volume and hence a decrease in ANP concentration.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Aging; Atrial Natriuretic Factor; Body Weight; Dehydration; Female; Humans; Male; Osmolar Concentration; Vasopressins

Topics: Body Water; Dehydration; Diabetes Insipidus; Diuretics; Drinking; Feedback; Glomerular Filtration Rate; Homeostasis; Humans; Inappropriate ADH Syndrome; Polyuria; Vasopressins; Water Intoxication

After 30 minutes spent in an upright posture six healthy male subjects underwent two 130-minute experiments in a supine posture, the first in thermoneutral conditions (TC) and the second, 15 days later, in a hot environment (HE) in order to obtain a water loss of 2.5% body weight. In thermoneutral conditions, the supine posture induced plasma volume expansion, resulting in slightly lowered plasma vasopressin (AVP) levels and higher plasma atrial natriuretic peptide (ANP) levels, compared to the values obtained in the upright posture (P less than 0.05). During hot environment, the sweating-induced dehydration led to a significant reduction of plasma volume expansion and to an increase in rectal temperature and plasma osmolality (P less than 0.05). Plasma vasopressin levels were higher at the end of the heat exposure (P less than 0.05) but natriuretic peptide levels did not change, compared to the values observed in the upright posture. These data suggest that plasma volume reduction induced by thermal dehydration may limit the natriuretic peptide release, which occurs after changing from the upright to a supine position.

Topics: Adult; Body Temperature; Body Water; Dehydration; Hot Temperature; Humans; Male; Natriuretic Agents; Osmolar Concentration; Plasma Volume; Posture; Vasopressins

We have investigated the rapid changes in plasma prolactin and arginine vasopressin (AVP) associated with water satiation in ruminants. Sheep deprived of water for 72 h were allowed voluntary access to ad libitum water. Each sheep drank approximately 5 liters in a single draft. This was performed in a head-down position, which was maintained for approximately 2-3 min and ceased rapidly with an abrupt movement to the upright position. During dehydration, plasma sodium, osmolality, and AVP all increased significantly, but prolactin was unaffected. On rehydration, AVP fell to basal levels within 5 min, but prolactin increased as a short pulse, after which it rapidly fell again. Plasma sodium and osmolality returned to predehydration levels within 6 h of satiation. A possible role of dopaminergic mechanisms in these responses was investigated by the administration of the dopamine agonist bromocriptine or the antagonist metoclopramide. Neither of these agents had any observable effects on the drinking behavior of the sheep during water satiation. During metoclopramide treatment, dehydration was associated with a marked fall in prolactin, and on rehydration there was a prompt and very marked increase in prolactin level. There was also an exaggerated increase of AVP during dehydration and a decrease on rehydration. Bromocriptine had relatively little effect on prolactin responses but prevented the drinking-associated inhibition of AVP, demonstrating an unexpected dissociation between AVP secretion and the stereotyped drinking response.

Topics: Animals; Behavior, Animal; Bromocriptine; Dehydration; Dopamine; Drinking Behavior; Female; Injections, Intramuscular; Metoclopramide; Osmolar Concentration; Prolactin; Satiation; Sheep; Sodium; Vasopressins

Magnocellular neurons synthesize vasopressin (VP) or oxytocin (OT) and release these hormones preferentially from the neural lobe during physiological stimulation. In the rat, VP is secreted preferentially during dehydration and hemorrhage, whereas OT is released without VP by suckling, parturition, stress, and nausea. Vasopressinergic neurons also synthesize and release dynorphin-related peptides--alpha- and beta-neoendorphin, dynorphin A (1-8) or (1-17), dynorphin B--which are agonists selective for kappa opiate receptors in the neural lobe. We proposed that one mechanism for preferential secretion of neurohypophysial hormones is that a dynorphin-related peptide(s) coreleased with VP inhibits selectively OT secretion from magnocellular neurons. We tested this hypothesis in conscious adult male Sprague-Dawley rats which were stimulated by either hypertonic saline administered intraperitoneally (2.5%, 20 ml/kg) or subcutaneously (1 M, 15 ml/kg) or by 24 h of water deprivation. Two approaches were used: (1) dynorphin-related peptides (0.02-20.4 mM) were injected intracerebroventricularly 1 min before decapitating the animal, and (2) the action of endogenous opioid peptides was blocked by injecting subcutaneously or intracerebroventricularly either naloxone or a selective kappa receptor antagonist, Mr 2266 or nor-binaltorphimine. VP and OT were measured by radioimmunoassay. After 24 h of water deprivation, the elevation in plasma [OT] but not [VP] was attenuated (p less than 0.05) by alpha-neoendorphin. Dynorphin A (1-8) also inhibited the release of OT and not VP after intraperitoneal administration of hypertonic saline. Blocking the action of endogenous opioid peptides at kappa receptors with Mr 2266 given peripherally (s.c.) elevated plasma [OT] but not [VP] after stimulation with hypertonic saline administered intraperitoneally or subcutaneously.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Benzomorphans; Dehydration; Dynorphins; Endorphins; Hypertonic Solutions; Injections, Intraventricular; Male; Naloxone; Naltrexone; Narcotic Antagonists; Neurons; Osmolar Concentration; Oxytocin; Peptide Fragments; Pituitary Gland, Posterior; Protein Precursors; Radioimmunoassay; Rats; Rats, Inbred Strains; Receptors, Opioid; Receptors, Opioid, kappa; Vasopressins

In rats euhydrated or dehydrated for two or four days the neurohypophysial vasopressin and oxytocin content was estimated. Rats were given intracerebroventricularly (i.c.v.) isoprenaline in a daily dose of 10 micrograms dissolved in 10 microliters of 0.9% sodium chloride. The neurohypophysial vasopressor and oxytocic activity diminished progressively during deprivation of water. A single dose of isoprenaline diminished the neurohypophysial content of vasopressin in euhydrated rats. In animals dehydrated for two or four days the depletion of neurohypophysial vasopressin storage (as brought about by osmoreceptor stimulation) was distinctly less marked under treatment with isoprenaline. The neurohypophysial oxytocin storage was diminished by a single dose of isoprenaline; on the contrary, during dehydration isoprenaline distinctly intensified the oxytocin depletion in the neurohypophysis.

Topics: Adrenergic Fibers; Animals; Dehydration; Isoproterenol; Male; Oxytocin; Pituitary Gland, Posterior; Rats; Rats, Inbred Strains; Synaptic Transmission; Vasopressins

Lactating goats were subjected to dehydration and to infusions of arginine vasopressin (AVP). Dehydration decreased milk production significantly but no changes were observed on the day of AVP infusion. The levels of AVP in plasma reached the same magnitude during both experimental procedures. AVP-immunoreactivity was immunocytochemically detected by light (peroxidase-antiperoxidase technique) and electron microscopy (immuno-Au technique on to glutaraldehyde-fixed, resin-embedded sections) in the mammary gland but not in the control experiments. In addition the cisternae of the rough endoplasmic reticulum in the secretory alveolar cells underwent significant swelling in response to the experimental procedures.

Topics: Animals; Dehydration; Female; Goat Diseases; Goats; Immunohistochemistry; Lactation; Mammary Glands, Animal; Microscopy, Immunoelectron; Osmolar Concentration; Vasopressins; Water Deprivation

The effect of rat brain natriuretic peptide (BNP) on drinking behaviour was examined in dehydrated and well-hydrated rats. Following dehydration for 18h, intracerebroventricular injections of 5 micrograms of rat BNP significantly reduced water consumption 0-2 h after the injections, but not 2-4 h afterwards. Rat BNP failed to decrease water intake in animals given water ad libitum. Thus, rat BNP is similar to alpha-atrial natriuretic polypeptide in that it only affects drinking in dehydrated rats. Following dehydration, plasma vasopressin levels were decreased by BNP, but BNP did not affect serum osmolality and electrolyte metabolism. These findings suggest that BNP may be involved in the central regulation of water consumption.

Topics: Animals; Blood; Chlorides; Dehydration; Drinking; Male; Natriuretic Peptide, Brain; Nerve Tissue Proteins; Osmolar Concentration; Rats; Rats, Inbred Strains; Sodium; Vasopressins

We studied 13 children subjected to elective tonsillectomy, 6 of whom (study patients) received supplemental intravenous isotonic saline during and after operation, and 7 of whom (controls) did not. Clinical and biochemical evidence of hypovolaemia was present in the control but not in the study patients. Plasma antidiuretic hormone (ADH) and urine osmolality were higher in controls (p less than 0.005 and p less than 0.05 respectively). Plasma sodium concentration and osmolality were similar in the two groups. We conclude that hypovolaemia is the principal stimulus to ADH release following surgery and that, in addition to replacement of observed losses of blood and other fluids by fluids of appropriate composition, hypovolaemia should be prevented by the administration of maintenance quantities of isotonic fluid, rather than exacerbated by fluid restriction, in patients in whom oral fluid intake is interrupted for more than a brief period. Hypotonic and sodium free fluids should be avoided because of the risk of hyponatraemia.

Topics: Catecholamines; Child; Child, Preschool; Dehydration; Fluid Therapy; Humans; Hyponatremia; Isotonic Solutions; Plasma Volume; Postoperative Complications; Sodium Chloride; Surgical Procedures, Operative; Tonsillectomy; Vasopressins

This study primarily sought to determine whether the role of vasopressin (VP) in maintenance of arterial blood pressure is enhanced in awake, chronically instrumented baboons after 68-72 h of dehydration. This question was approached by pharmacologically blocking vasopressin V1-receptors in euhydrated and dehydrated baboons with or without a normally functioning renin-angiotensin system (RAS). VP blockade during dehydration produced a rapidly occurring (within 5 min), statistically significant (P less than 0.05) decrease in mean arterial pressure (MAP) of 5 +/- 1 mmHg in the RAS-intact condition and an identical decline in MAP (5 +/- 1 mmHg) during blockade of the RAS by captopril, an angiotensin I-converting enzyme inhibitor. At 15 min after induction of VP blockade, heart rate was elevated by 9 +/- 2 beats/min in the RAS-intact condition and by 20 +/- 5 beats/min in the RAS-blocked condition. In addition, VP blockade in the dehydrated state produced small and equal increases in hindlimb vascular conductance in RAS-intact and RAS-blocked conditions. None of these cardiovascular changes were produced by VP blockade in the euhydrated state. RAS blockade produced modest declines in MAP in both hydration states, but the fall was larger by 7 +/- 4 mmHg in the dehydrated state. Thus both VP and the RAS contribute to the maintenance of arterial blood pressure during dehydration in the conscious baboon.

Topics: Animals; Blood Pressure; Captopril; Dehydration; Heart Rate; Ilium; Male; Papio; Receptors, Angiotensin; Receptors, Vasopressin; Reference Values; Regional Blood Flow; Vasopressins

To investigate the influence of various peptides on control of dehydration-induced drinking, water intake elicited by overnight water deprivation was analyzed in groups of male rats after intracerebroventricular (third ventricle, icv) injection of 2 microliters of normal rabbit serum or an equal volume of antiserum directed against angiotensin II (Ab-AII), atrial natriuretic peptide, vasopressin, or oxytocin. There was no difference in water intake after normal rabbit serum and antiserum injections when water was offered immediately after icv injections. Water intake was greatly reduced by Ab-AII when water was offered 1 hr and 3 hr after icv injection. The other antisera were partially effective only when water was offered 3 hr after icv injection. The dipsogenic effect of icv injection of AII in normally hydrated rats was reduced only by icv injection of Ab-AII 3 hr before and not by the other antisera. Ab-AII injected icv had no effect on the drinking that occurred just before and after the onset of darkness and that was associated with eating (prandial drinking). The results indicate that AII is primarily responsible for dehydration-induced drinking, and the other peptides may play a permissive role since their antisera were partially effective, with longer latencies after antiserum injection, which is perhaps the result of gradual diffusion to effective sites within the hypothalamus. In contrast, endogenous AII appears to play little, if any, role in prandial drinking.

Topics: Angiotensin II; Animals; Antigen-Antibody Reactions; Atrial Natriuretic Factor; Dehydration; Drinking Behavior; Hypothalamus; Male; Microinjections; Oxytocin; Rats; Vasopressins; Water-Electrolyte Balance

The effects of naloxone, an opioid antagonist, on arginine vasopressin (AVP) secretion were examined in conscious unrestrained rats under both basal and stimulated conditions. Intravenous injection of naloxone in a dose of 0.1 mg/kg did not significantly affect the basal plasma AVP level. However, 0.5 or 2.5 mg/kg naloxone significantly raised the basal AVP level in euhydrated rats. Naloxone (0.5 mg/kg) significantly enhanced AVP secretion after 72-h water deprivation. However, the enhancement was more prominent in euhydrated rats than in dehydrated rats. Pretreatment with naloxone (0.5 mg/kg) also significantly prolonged AVP secretion induced by intracerebroventricular injection of angiotensin-II (100 ng). Moreover, naloxone (0.5 mg/kg) significantly increased AVP secretion induced by intracerebroventricular injection of carbachol (10 ng). Naloxone (0.5 mg/kg) altered neither basal blood pressure nor the angiotensin-II-induced pressor response, but augmented the carbachol-induced pressor response. This suggests that facilitation of AVP secretion by naloxone is not due to a reflex mechanism resulting from decreased blood pressure. These results indicate that endogenous opioid peptides exert a tonic inhibitory control on AVP secretion in rats.

Topics: Angiotensin II; Animals; Blood Pressure; Carbachol; Consciousness; Dehydration; Endorphins; Heart Rate; Male; Naloxone; Narcotic Antagonists; Rats; Rats, Inbred Strains; Receptors, Opioid; Vasopressins

Fluid overload and dehydration are potentially serious physiologic perturbations. Their effects on the pharmacodynamics of drugs are essentially unknown. This investigation was designed to determine the effects of acute fluid overload or water deprivation on the hypnotic activity of phenobarbital and on the neurotoxicity of theophylline in male Lewis rats. In the first experiment, 5% dextrose in water (D5W) was infused i.v. in an amount equal to 5 or 10% of body weight and phenobarbital was infused immediately thereafter until the onset of loss of righting reflex (LRR). The total infused dose and the serum and cerebrospinal fluid (CSF) concentrations of phenobarbital at that time were significantly lower than in control animals. When phenobarbital was infused about 2.5 hr after D5W, the infused dose and the serum and CSF concentrations of phenobarbital at LRR were normal. When the rats received D5W and an injection of vasopressin, 25 I.U./kg, or vasopressin only, the infused dose and the serum and CSF concentrations of phenobarbital at LRR were significantly lower than in controls despite the 2.5-hr interval between the respective pretreatments and the phenobarbital infusion. Water deprivation for 24 or 48 hr had no significant effect on phenobarbital dose and concentrations at LRR. Intravenous infusion of D5W to 10% of body weight immediately or 2.5 hr before theophylline infusion had no significant effect on the total infused dose and the serum and CSF concentrations of theophylline at onset of maximal seizures. This lack of effect occurred despite appreciable hyponatremia and hypomagnesemia immediately after D5W infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Dehydration; Glucose; Male; Phenobarbital; Rats; Rats, Inbred Lew; Seizures; Theophylline; Vasopressins; Water-Electrolyte Imbalance

Inner medullary methylamine [glycerophosphorylcholine (GPC) and glycine betaine (betaine)] and polyol [sorbitol and myo-inositol (inositol)] osmolytes were measured in water-restricted and antidiuretic hormone (ADH)-infused Brattleboro (DI) rats. Compared with DI rats allowed water ad libitum, rats dehydrated for 3 days had higher urinary osmolality (Uosmol) (812 vs. 239 mosmol/kgH2O) and plasma osmolality (Posmol) (333 vs. 296 mosmol/kgH2O). Dehydration reduced betaine content (36 vs. 66 nmol/mg protein) but had no significant effect on GPC, sorbitol, or inositol. In separate protocols, DI rats, allowed water ad libitum, were infused for either 3 or 12 days with either ADH in saline (+ADH) or saline alone (-ADH). Compared with -ADH controls, 3- or 12-day ADH-infused rats were antidiuretic (Uosmol, 1,000-1,300 mosmol/kgH2O) but not dehydrated (Posmol, 297-300 mosmol/kgH2O). Three days of ADH infusion caused an increase in GPC (340%), betaine (80%), and sorbitol (248%) but not in inositol. After 12 days of ADH, further increases were observed in GPC (730%) and sorbitol (870%); inositol was also elevated (170%), whereas betaine was unchanged. Consequently, the total osmolyte content was significantly higher in +ADH than in -ADH [449 vs. 256 (3 days) and 778 vs. 199 (12 day) nmol/mg protein], whereas total osmolyte levels in dehydrated and control rats were similar (222 vs. 219 nmol/mg protein).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Dehydration; Infusion Pumps; Kidney Medulla; Osmolar Concentration; Rats; Rats, Brattleboro; Rats, Mutant Strains; Time Factors; Vasopressins; Water Deprivation

Six pony mares deprived of water for 24 hours showed significant increases in plasma vasopressin (2.8 pg/ml) and osmolality (9 mosmol/kg). When water was made available the ponies drank rapidly (5 of 6 drank to satiety within 90 seconds) and corrected their fluid deficits precisely. Vasopressin did not return to predehydration levels until osmolality did after 15 minutes of access to water. The horse differs from rodents and humans, but is similar to pigs in that vasopressin levels do not fall before osmolality returns to normal. Oropharyngeal factors, therefore, may not be as important in vasopressin release in horses as in other species.

Topics: Animals; Behavior, Animal; Dehydration; Drinking Behavior; Female; Horses; Osmolar Concentration; Reaction Time; Time Factors; Vasopressins

Hyponatremia, in patients with central nervous system disease, can be attributable to impaired free water excretion (syndrome of inappropriate secretion of antidiuretic hormone) or to excessive sodium excretion (cerebral salt wasting). We present a patient with a parietal glioma and hyponatremia characterized by salt wasting and dehydration. Rehydration and sodium repletion corrected the sodium and volume deficits; withdrawal of supplemental sodium resulted in recurrence of dehydration and hyponatremia. We determined sodium and water balance and measured plasma atriopeptin, antidiuretic hormone, and aldosterone. Plasma atriopeptin ranged from 8 to 44 pg/mL (normal, less than 45 pg/mL); antidiuretic hormone was not elevated at 4 to 5 pg/mL, and aldosterone was slightly elevated at 1040.25 pmol/L. The concentrations of these hormones could not directly explain the natriuresis; interactions with neural or other humoral factors may be involved. In evaluating such patients, careful attention to sodium and water balance is important to guide appropriate therapy.

Topics: Adult; Aldosterone; Brain Neoplasms; Dehydration; Glioma; Humans; Hyponatremia; Male; Sodium; Vasopressins; Water-Electrolyte Balance

Alzheimer's disease is a progressive deterioration of neuropsychological functioning. One of the main neuropathological correlates of the disease is a drop-out of cholinergic neurons within the central nervous system. The neuropeptide that is responsible for water homeostasis and defense against dehydration, vasopressin, is also under direct cholinergic control. Several studies have suggested that in Alzheimer's disease there has been a trend toward lower vasopressin levels than in age-matched controls. In order to improve discrimination of normal from diminished vasopressin levels, nine subjects with Alzheimer's disease (mean age 65 +/- 2 years) and nine age- and sex-matched controls (68 +/- 3 years) underwent a mild provocative challenge of overnight fluid restriction. Individuals with Alzheimer's disease had a greater degree of dehydration, with overnight serum osmolality of 313 +/- 4 vs 300 +/- 3 Mosmol/kg, P = .01, and diminished "thirst" as measured by water ingested in one hour of ad libitum water intake. Eight of the nine with Alzheimer's disease had levels of vasopressin which, by extrapolation, appear to be subnormal for their serum osmolalities, whereas seven of the nine control subjects has vasopressin levels within or above the reference range (P less than .05). Elderly individuals with Alzheimer's disease may be at increased risk of dehydration during periods of fluid restriction due to the loss of normal physiological responses of "thirst" and vasopressin secretion.

Topics: Aged; Alzheimer Disease; Cognition; Dehydration; Female; Humans; Male; Middle Aged; Osmolar Concentration; Sex Characteristics; Thirst; Vasopressins

The contiguous three lobe of the pituitary gland have different endocrine functions and vascular bed. This study was designed to investigate the effects of dehydration, which stimulates the secretion of vasopressin, on the pituitary microcirculation. Male Sprague-Dawley rats, weighing 300-380 g, were divided into two groups. Twenty three rats were allowed free access to food and water, and 24 rats had free access to food but were deprived of water for 5 days. Capillary solute transfer (K), plasma volume (Vp) and erythrocyte volume (Ve) in each pituitary lobe were determined for both control and dehydrated rats. Quantitative autoradiographic techniques were used to measure the K with 14C-alpha-aminoisobutyric acid (AIB, a small neutral amino acid), the Vp with 125I-albumin and the Ve with 51Cr-erythrocytes. Body weight was lower (-23%) and the arterial hematocrit was higher (+22%) in the dehydrated rats. In the lobes of the control pituitary gland, the order of K from the highest to the lowest was posterior much greater than anterior greater than intermediate lobe. K was increased by several folds only in the posterior lobe in dehydrated rats (p less than 0.05). Even under normal hydrated conditions, K for AIB in the posterior lobe was several hundreds times greater than in cerebral gray matter structures. The rank of Vp and Ve in each lobe of normal animals was about the same order and anterior greater than posterior much greater than intermediate. Normal microvascular Vp in the anterior and posterior lobes was 5-10 times larger than in cerebral gray matter.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aminoisobutyric Acids; Animals; Autoradiography; Capillary Permeability; Carbon Radioisotopes; Dehydration; Erythrocyte Volume; Male; Microcirculation; Pituitary Gland; Plasma Volume; Rats; Rats, Inbred Strains; Vasopressins

The roles of the autonomic nervous system, vasopressin, and angiotensin II in support of blood pressure were evaluated in seven conscious, resting dogs while hydrated or dehydrated. Mean arterial blood pressure (MAP) was monitored, and the dogs were given hexamethonium to block autonomic ganglia. Thirty minutes later, they were given captopril, and after another 30 min, a vasopressin V1 antagonist, d(CH2)5TyrMeAVP, was given. The order okf administration of captopril and d(CH2)5TyrMeAVP was alternated in different experiments. Hexamethonium had no effect on steady-state MAP in either hydrated or dehydrated dogs. In hydrated dogs, the average MAP was 100 mmHg; d(CH2)5TyrMeAVP decreased MAP by approximately 12 mmHg, and captopril decreased MAP by 24 mmHg. The magnitude of the effect of these two inhibitors was independent of the order of their administration. Dehydration doubled the effect of d(CH2)5TyrMeAVP on MAP but had no effect on the response to captopril. The results suggest that 1) autonomic function is not essential for maintenance of arterial blood pressure in resting dogs; 2) during autonomic ganglionic blockade, arterial blood pressure is supported by both angiotensin II and vasopressin; and 3) dehydration increases the role of vasopressin in control of blood pressure.

Topics: Angiotensin II; Animals; Arginine Vasopressin; Blood Pressure; Captopril; Dehydration; Dogs; Female; Ganglia, Autonomic; Heart Rate; Hexamethonium; Hexamethonium Compounds; Male; Reference Values; Renin; Vasopressins

Human alpha-atrial natriuretic peptide (h-alpha ANP) makes the urine of dehydrated volunteers hypotonic to plasma despite high circulating concentrations of antidiuretic hormone. Urinary dilution with h-alpha ANP also occurs in subjects receiving indomethacin. Therefore, h-alpha ANP antagonises effects of antidiuretic hormone on distal tubular V2-receptors in man, probably without involving prostaglandins.

Topics: Arginine Vasopressin; Atrial Natriuretic Factor; Blood; Dehydration; Diuresis; Humans; Indomethacin; Male; Osmolar Concentration; Receptors, Angiotensin; Receptors, Vasopressin; Renin; Urine; Vasopressins

Dehydrated patients usually present with an elevated serum urea level, owing in part to increased renal reabsorption of urea mediated by antidiuretic hormone (ADH). We carried out a study to examine whether, during dehydration, the variations in the serum urea level could discriminate patients with central diabetes insipidus (CDI) from those with dehydration not due to CDI. We studied retrospectively 27 episodes of dehydration in 23 patients with CDI and 14 episodes in 14 patients without CDI. The mean serum urea level was 2.9 mmol/L in the CDI group and 15.4 mmol/L in the patients without CDI (p less than 0.001); the mean serum sodium level was 155 mmol/L in both groups. All the patients with CDI had a sodium/urea ratio greater than 24.2, whereas the ratio was less than 21.7 in all the patients without CDI. In the patients with CDI a positive correlation was found between the magnitude of diuresis and the percentage decrease in the serum urea level compared with the level before dehydration (p less than 0.001). In the patients with CDI the serum urea level returned to the level before dehydration after the administration of vasopressin; a striking increase in the clearance of urea, which exceeded the creatinine clearance, was observed during dehydration in the three patients in whom clearance studies were done. The results suggest that serum urea values can be used to distinguish patients dehydrated because of CDI from those with hypertonic dehydration but without ADH deficiency and that during dehydration the net reabsorption of urea is dependent on the renal action of ADH.

Topics: Adult; Creatinine; Dehydration; Diabetes Insipidus; Female; Fluid Therapy; Humans; Hypernatremia; Male; Middle Aged; Osmolar Concentration; Prospective Studies; Retrospective Studies; Urea; Vasopressins

The contributions of the kidneys, the small intestine and the lower intestine (rectum plus cloaca) to water conservation during dehydration in unanaesthetized, unrestrained house sparrows (Passer domesticus) were assessed. Thirty hours of acute dehydration resulted in a 12% loss in body mass and a significant increase in plasma osmolality. Glomerular filtration rate declined by 55%, from 7.7 to 3.5 ml/h, and urine flow rate delined by more than 80%, from 0.2 to 0.03 ml/h. These changes are likely attributable to a large increase in plasma levels of arginine vasotocin during dehydration, from less than 26 pg/ml in hydrated birds to greater than 200 pg/ml after 30 h dehydration. Flow of water from the ileum to the lower intestine was reduced during dehydration, primarily because of a reduced flow of dry matter (with no significant reduction in water content). The rate of water loss in the excreta declined from 0.2 ml/h in hydrated birds to 0.04 ml/h in dehydrated birds. The rate of water reabsorption in the lower intestine (equal to the rate of water loss in the excreta minus the combined rates of inflow into the lower intestine from the urine and the ileal contents) slightly exceeded the rate of water flow from the ileum in both hydrated and dehydrated birds. We suggest that much of the water reabsorbed in the lower intestine of hydrated birds derives from the urine, but that primarily water from ileal contents is reabsorbed in dehydrated birds. That is, urine undergoes significant post-renal modification in hydrated but not dehydrated house sparrows.

Topics: Animals; Birds; Chickens; Cloaca; Dehydration; Ducks; Glomerular Filtration Rate; Intestine, Small; Intestines; Kidney; Rectum; Urodynamics; Vasopressins; Vasotocin; Water-Electrolyte Balance

This study, carried out in two parts, sought to determine the importance of vasopressin (VP), the renin-angiotensin system (RAS), and the sympathetic nervous system in the dehydration-produced attenuation of hindlimb (cutaneous) vasodilation during environmental heating (EH). Baboons, chronically instrumented for blood sampling and for measurement of mean iliac blood flow (MIBF), arterial pressure, and core temperature (Tc), were subjected to EH while in euhydrated and dehydrated (64-72 h of water deprivation) states. EH consisted of exposure to an elevated ambient temperature (40-42 degrees C) until Tc reached 39.5 degrees C. In part I, indexes of the above vasoconstrictor systems were measured. Base-line plasma renin activity (PRA) and VP and norepinephrine concentrations were all significantly elevated by dehydration. In addition, the increase in PRA during EH was accentuated by dehydration. In part II, the effects of blockades of the RAS, the pressor action of VP, and the innervation of the hindlimb on hindlimb vasodilation during EH were assessed. None of these blockades, singly or together, reversed the dehydration-produced attenuation of the increase in MIBF during EH. Thus we conclude that other mechanisms are responsible for the dehydration-produced attenuation of cutaneous vasodilation in baboons during EH.

Topics: Animals; Dehydration; Epinephrine; Hemodynamics; Hot Temperature; Leg; Male; Norepinephrine; Papio; Regional Blood Flow; Renin; Renin-Angiotensin System; Sympathetic Nervous System; Vasoconstriction; Vasodilation; Vasopressins; Water Deprivation

The circadian rhythm and dehydration-induced response of vasopressin (AVP) levels in rat cerebrospinal fluid (CSF) were studied after lesions had been made in the paraventricular (PVN) and suprachiasmatic (SCN) nuclei. The rhythmic fluctuation of AVP levels in CSF was abolished after SCN lesions, whereas lesions of the PVN had no effect. Dehydration seems to increase AVP levels in CSF of both sham-operated and lesioned animals. These data further suggest that the circadian rhythm of AVP in CSF is preferentially generated by SCN. In contrast, several areas of the brain may contribute to the overall AVP levels in CSF, both under normal physiological conditions and under osmotic stress.

Topics: Animals; Circadian Rhythm; Dehydration; Male; Paraventricular Hypothalamic Nucleus; Rats; Rats, Inbred Strains; Suprachiasmatic Nucleus; Vasopressins

Rats euhydrated and dehydrated for two days were given intracerebroventricularly (i.c.v.) propranolol hydrochloride in a daily dose of 10 micrograms. In euhydrated rats the single dose of propranolol diminished significantly the vasopressin and oxytocin content in the neurohypophysis. On the contrary, in animals dehydrated for two days the depletion of the vasopressin and oxytocin neurohypophysial storage was distinctly less marked during i.c.v. treatment with propranolol.

Topics: Animals; Dehydration; Injections, Intraventricular; Male; Oxytocin; Pituitary Gland, Posterior; Propranolol; Rats; Rats, Inbred Strains; Vasopressins

Topics: Bone Marrow Transplantation; Bronchial Neoplasms; Carcinoma, Small Cell; Cyclophosphamide; Dehydration; Diabetes Insipidus; Humans; Kidney Diseases; Liver Neoplasms; Male; Middle Aged; Vasopressins

One physiological role for endogenous opioid peptides is to attenuate the release of oxytocin (OT) from the hypothalamo-neurohypophysial system during dehydration and hemorrhage when vasopressin maintains fluid balance and blood pressure. During lactation, OT, which stimulates milk ejection, is released without vasopressin. The influence of endogenous opioid peptides on OT release during suckling has been studied primarily in animals anesthetized with urethane. In addition to anesthesia, urethane dehydrates the animal by elevating plasma osmolality and reducing cardiovascular volume. Thus, we examined in lactating rats the response of the magnocellular neuroendocrine system to dehydration and the role of endogenous opioid peptides in regulating OT release during suckling under conditions of altered fluid balance in conscious and urethane-anesthetized rats. Release of OT in response to an increase in plasma osmolality or a decrease in blood volume was attenuated during lactation in both conscious and anesthetized rats. Blockade of opiate receptors with naloxone (5 mg/kg) did not alter suckling-induced release of immunoreactive OT in conscious, normally hydrated rats, but did augment hormone release after urethane (1.1 g/kg, ip) or after osmotic stimulation with hypertonic sodium chloride (2.5%; 20 ml/kg, ip). During dehydration, the combination of decreased responsiveness of oxytocinergic neurons to osmotic stimulation and inhibition of OT release by opioid peptides may be important in the lactating rat for conserving pituitary stores of OT needed for milk ejection.

Topics: Anesthesia; Animals; Blood; Dehydration; Female; Lactation; Naloxone; Osmolar Concentration; Oxytocin; Pregnancy; Rats; Rats, Inbred Strains; Saline Solution, Hypertonic; Urethane; Vasopressins; Water-Electrolyte Balance

The act of drinking ameliorates thirst and inhibits the secretion of vasopressin before changes in extracellular fluid volume or osmolality in both animals and man. We evaluated whether this reflex inhibition of vasopressin secretion might be due to the presence of oropharyngeal receptors in humans. After dehydration, normal subjects (n = 4) were allowed to suck on ice chips for 30 min. Despite the absence of changes in plasma sodium (Na+) or osmolality, the mean plasma vasopressin level decreased promptly within 10 min from 2.8 to 1.8 pg/mL, and it remained low for 30 min after ice ingestion. When the dehydration protocol was repeated with the subjects receiving 100 mL water (25 C) for 30 min rather than ice chips, plasma vasopressin levels did not change. These data demonstrate that activation of cold-sensitive oropharyngeal receptors results in inhibition of vasopressin secretion independently of osmotic or gastric factors. In a second study 0.2 mL/kg X min 3% NaCl was administered for 90 min as a second stimulus to vasopressin secretion, and ice chips were given during the last 30 min of infusion. Plasma vasopressin levels increased steadily to 3.3 +/- 0.5 (+/- SEM) pg/mL by 45 min, and despite ice ingestion increased further to 4.6 +/- 0.8 pg/mL by 90 min. Consequently, hypertonicity appears to be a stronger stimulus to vasopressin release, since the suppressive effect of stimulation of oropharyngeal receptors with ice was not evident during the NaCl infusion. Finally, no changes in vasopressin levels were found in subjects holding concentrated NaCl solutions in their mouths for 30 min, indicating that the oropharyngeal receptors are not responsive to local changes in osmolality. The presence of such cold-sensitive oropharyngeal receptors may explain the desire of severely dehydrated patients, e.g. patients with diabetes insipidus, for cold liquids.

Topics: Adult; Cold Temperature; Dehydration; Humans; Male; Oropharynx; Sensory Receptor Cells; Thirst; Vasopressins; Water

Vasopressin is the primary physiological factor regulating renal water reabsorption in mammals. Inhibitors of vasopressin-stimulated water reabsorption have previously been used as water diuretic agents in both experimental animals and man. The present studies describe and characterize the pharmacological effects of the potent vasopressin antagonist desGly d(CH2)5D-Tyr(Et)VAVP (SK&F 101926) and related analogs on renal water and solute excretion in conscious rats. Administration of SK&F 101926 was associated with dose-dependent increases in renal water excretion in conscious hydropenic rats. A selective vasopressin pressor (V1) antagonist (SK&F 100273) was inactive as a diuretic agent in these tests. SK&F 101926 antagonized, in a competitive fashion, exogenous vasopressin-stimulated antidiuresis in conscious water-loaded rats. Only modest increases in renal excretion of Na+, K+, and urea were observed when SK&F 101926 was administered. No changes in endogenous creatinine excretion were associated with the administration of SK&F 101926, suggesting that this drug does not affect glomerular filtration rate. The rank order of bioequivalency of alternative routes of administration of SK&F 101926 was intraperitoneal = intravenous = intramuscular = subcutaneous greater than intranasal much greater than rectal, ocular, and oral. SK&F 101926 (20 micrograms/kg/day) was effective in blocking the development of hyponatremia in a rat model of the syndrome of inappropriate antidiuretic hormone (SIADH). SK&F 100273 (100 micrograms/kg) hastened the onset of endotoxin-associated shock in rats. We conclude that SK&F 101926 is a potent water diuretic (aquaretic) agent in rats. The mechanism of action is most probably antagonism of vasopressin at renal epithelial (V2) receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Arginine Vasopressin; Dehydration; Diuresis; Dose-Response Relationship, Drug; Inappropriate ADH Syndrome; Male; Osmolar Concentration; Rats; Shock, Septic; Vasopressins

The present study was designed to investigate in rats the influence of converting enzyme inhibition with captopril on blood pressure, plasma urea, plasma renin concentration (PRC), plasma aldosterone and plasma vasopressin, and to define the interrelationships between PRC and these variables during equal degrees of either hyponatraemic (furosemide, 40 mg/kg for 2 days) or hypernatraemic (48-h water deprivation) dehydration. Chronic treatment with captopril (40 mg/kg daily) decreased blood pressure by 19% in normally hydrated treated rats, by 27% in water-deprived treated rats and by 40% in furosemide-treated rats. Plasma renin concentration, plasma aldosterone and plasma vasopressin were increased during both hypo- and hypernatraemic dehydration. Captopril decreased plasma aldosterone in water-deprived and furosemide-treated rats, whereas plasma vasopressin was unchanged. The significant correlation observed between plasma aldosterone and PRC in non-treated rats persisted in treated rats, the same level of plasma aldosterone being observed at values of PRC 10 times higher. On the other hand, the correlation between plasma vasopressin and PRC did not persist in captopril-treated rats. An increase in plasma urea was observed in both water-deprived treated rats and furosemide-treated rats. These data indicate that during hypo- and hypernatraemic dehydration, the renin-angiotensin system plays a role in regulating blood pressure, urea elimination and plasma aldosterone, but vasopressin regulation is not modified by its inhibition.

Topics: Aldosterone; Angiotensin-Converting Enzyme Inhibitors; Animals; Blood Pressure; Captopril; Dehydration; Hypernatremia; Hyponatremia; Kidney; Male; Rats; Renin; Renin-Angiotensin System; Urea; Vasopressins

Binding sites for rat atrial natriuretic peptide (6-33) (ANP) were quantitated in the subfornical organ of chronically dehydrated homozygous Brattleboro rats unable to synthesize vasopressin; heterozygous Brattleboro rats, their controls, Long Evans rats and Long Evans rats after 4 days of water deprivation. Brain sections were incubated in the presence of 125I-ANP and the results analyzed by autoradiography coupled to computerized microdensitometry and comparison to 125I-standards. Brattleboro rats and water deprived Long Evans rats presented a higher number of ANP binding sites than their normally hydrated controls. Our results suggest a role of ANP binding sites in the subfornical organ in the central regulation of fluid balance and vasopressin secretion.

Topics: Animals; Atrial Natriuretic Factor; Autoradiography; Dehydration; Frontal Lobe; Male; Peptide Fragments; Rats; Rats, Brattleboro; Receptors, Atrial Natriuretic Factor; Receptors, Cell Surface; Vasopressins; Water Deprivation; Water-Electrolyte Balance

If plasma vasopressin (PVP), plasma renin (PRA), and plasma aldosterone (PA) responses to change in posture are mediated only by alterations in intrathoracic baroreceptor activity, hydration status should have minimal influence on these responses. To test this hypothesis, six male subjects underwent 45 min of 70 degree head-up tilt (HUT) following 26 h dehydration, and again, 105 min later, following rehydration. Compared with preceding supine hydrated control values, PVP, PRA, and PA increased (p less than 0.001) during dehydrated HUT, but only PVP and PRA increased during rehydrated HUT (p less than 0.001). The dissociation during rehydrated HUT of PRA and PA may have been related more to the reduction (p less than 0.001) in plasma potassium concentration than to the accompanying decrease (p less than 0.001) in plasma osmolality and sodium concentration. Although increases in PVP and PRA during HUT were attenuated (p less than 0.01) following rehydration, this attenuation was associated with the absence of symptoms of overt hypotension following rehydration. However, since rehydration did not abolish the increases in PVP and PRA induced by HUT, it is concluded that the present observations support the concept of intrathoracic baroreceptor involvement in the regulation of vasopressin secretion and renin release.

Topics: Adult; Aldosterone; Blood Volume; Dehydration; Humans; Male; Middle Aged; Plasma Volume; Posture; Potassium; Pressoreceptors; Renin; Sodium; Time Factors; Vasopressins; Water-Electrolyte Balance

Enkephalins are found in the posterior pituitary, can alter vasopressin secretion, and have greater pressor effects in spontaneously hypertensive rats (SHR) than in Wistar-Kyoto (WKY) rats. Measurement of the plasma methionine-enkephalin concentration (PMet-Enk) has provided equivocal results in humans and has not been reported in rats. We have developed a highly specific and sensitive Met-Enk radioimmunoassay and determined that Met-Enk circulates in rats but that PMet-Enk is no different between SHR and WKY rats (7.6 +/- 0.8 and 9.2 +/- 0.8 pg/ml, respectively). Water deprivation for 48 h increased the plasma vasopressin concentration (PADH) and 24-h urinary vasopressin excretion (UADHV) in SHR and WKY rats, but PMet-Enk was not altered. There were no differences in PADH and UADHV between SHR and WKY rats in either the euhydrated or dehydrated state. These results suggest that it is unlikely that circulating Met-Enk contributes importantly to the maintenance of hypertension in SHR. There was also no evidence for a greater secretion of vasopressin in SHR than in WKY rats, in contrast to previous reports.

Topics: Animals; Blood Pressure; Body Weight; Dehydration; Diuresis; Enkephalin, Methionine; Heart Rate; Hypertension; Male; Osmolar Concentration; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Sodium; Vasopressins

A 17-year-old schizophrenic developed severe hypernatremia during a period of psychosis. The thirst-deficient abnormality that caused this hypernatremia resolved when his psychosis improved. The primary disorders causing a thirst deficiency leading to hypernatremia fall into three categories: lesions of the central nervous system, mineralocorticoid excess, and drug side effects. None of these disorders was found in our patient. We conclude that psychosis can severely impair the thirst mechanism directly.

Topics: Adolescent; Dehydration; Humans; Hypernatremia; Male; Osmolar Concentration; Schizophrenia; Thirst; Vasopressins

We have shown, using the opiate receptor antagonist naltrexone, that endogenous opioid peptides inhibit the release of oxytocin (OT), but not of vasopressin (AVP), from the hypothalamo-neurohypophysial system during dehydration. The stimulus for the release of neurohypophysial hormones during dehydration is both hypovolemia and increased plasma osmolality. The aims of this study were to determine whether opioid peptides inhibit OT secretion during an osmotic stimulus alone and, if so, to study the ontogeny of opiate inhibition of OT and AVP release during osmotic stimulation. Effects of endogenous opioid peptides were evaluated by injecting naloxone into immature and adult rats. Hypertonic saline was used as the osmotic stimulus. Adult male rats were injected sc with normal saline (0.85%; 1 ml/kg BW) or naloxone (5 mg/kg BW), followed 5 min later by normal or hypertonic (1 M) saline (15 ml/kg BW). After 170 min, a second injection of saline or naloxone was given; animals were decapitated 10 min later. Immature male and female rats at 2, 8, 21, and 30 days of age received 0.85% saline (1 ml/kg BW) or naloxone (5 mg/kg BW) ip 5 min before normal or hypertonic (2.5%) saline (20 ml/kg BW, ip). Pups were decapitated 15 min later. AVP and OT were measured by RIA in extracts of plasma, pituitaries, and hypothalami. In control rats, the contents of AVP and OT increased with age in both the pituitary and hypothalamus, attaining adult levels by day 21 for AVP and by day 30 for OT. In contrast, plasma concentrations of both AVP and OT were highest in 8-day-old rats and decreased thereafter to adult levels by 30 days of age. Hypertonic saline raised plasma osmolality 9-16 mosmol/kg H2O, increased AVP and OT concentrations in plasma of adults and immature rats at 2, 8, 21, and 30 days of age, and reduced pituitary stores of OT in adult animals. Blocking the action of opioid peptides with naloxone during osmotic stimulation augmented the rise in plasma OT in rats of all ages but further elevated plasma AVP only in immature rats. In adult animals, blocking opiate receptors with naloxone enhanced the depletion of OT stores from the pituitary, but did not affect the AVP content. We conclude that in the adult rat, endogenous opioid peptides inhibit OT release during osmotic stimulation, thereby allowing preferential release of AVP.(ABSTRACT TRUNCATED AT 400 WORDS)

Topics: Animals; Dehydration; Endorphins; Hypertonic Solutions; Hypothalamus; Male; Naltrexone; Osmosis; Oxytocin; Pituitary Gland, Posterior; Rats; Rats, Inbred Strains; Sodium Chloride; Vasopressins

The possibility that metoclopramide (MCP), a potent stimulator of aldosterone secretion, might influence vasopressin secretion in man was studied. MCP (10 mg, iv) increased plasma vasopressin (mean +/- SD) from 1.3 +/- 0.1 to 2.4 +/- 0.1 pg/ml at 10 min and to 2.65 +/- 0.1 pg/ml at 20 min (P less than 0.01) in 10 recumbent normal subjects. No changes in plasma osmolality or peripheral hemodynamics, which might have accounted for the increase in vasopressin, were found. Sulpiride (100 mg iv), haloperidol (2 mg, iv), and domperidone (20 mg, iv), three chemically unrelated antidopaminergic agents, as well as TRH (200 micrograms, iv), failed to modify plasma vasopressin, thus suggesting that the MCP effect on vasopressin is not linked to its antidopaminergic and/or PRL-releasing properties. MCP also was effective in releasing vasopressin in 5 dehydrated subjects, in whom plasma vasopressin increased from 1.9 +/- 0.2 to 3.1 +/- 4 pg/ml (P less than 0.05), and in 5 subjects during steady state water diuresis, in whom free water excretion decreased from 9 to 1 ml/min (P less than 0.01) and plasma vasopressin increased from 0.3 +/- 0.1 to 1.2 +/- 0.2 pg/ml (P less than 0.05). No changes in either vasopressin secretion or free water excretion occurred in 4 patients with severe central diabetes insipidus. These results suggest that MCP stimulates the release of biologically active vasopressin in man.

Topics: Adult; Blood Pressure; Dehydration; Diabetes Insipidus; Diuresis; Female; Heart Rate; Humans; Male; Metoclopramide; Middle Aged; Osmolar Concentration; Vasopressins; Water

To determine the effect of hydration on the early osmotic and intravascular volume and endocrine responses to water immersion the hematocrit, hemoglobin, plasma renin activity (PRA), and plasma electrolyte, aldosterone (PA), and vasopressin (PVP) concentrations were measured during immersion following 24-h dehydration; these were compared with corresponding values following rapid rehydration. Six men and one woman (age 23-46 yr) underwent 45 min of standing immersion to the neck preceded by 45-min standing without immersion, first dehydrated, and then 105 min later after rehydration with water. Immersion caused an isotonic expansion of the plasma volume (P less than 0.001), which occurred independently of hydration status. Suppression of PRA (P less than 0.001) and PA (P less than 0.001) during both immersions also occurred independently of hydration status. Suppression of plasma vasopressin was observed during dehydrated immersion (P less than 0.001) but not during rehydrated immersion. It is concluded that plasma tonicity is not a factor influencing PVP suppression during water immersion.

Topics: Adult; Aldosterone; Angiotensin I; Blood Proteins; Dehydration; Electrolytes; Female; Fluid Therapy; Hematocrit; Humans; Immersion; Male; Middle Aged; Plasma Volume; Vasopressins

Twelve steers of three different breeds were exposed to five feed and water regimes in order to characterize changes in plasma antidiuretic hormone (ADH) concentrations. No breed differences were found in plasma ADH concentration. Plasma ADH concentration rose (4.2 to 22.0 pg/ml) during dehydration. By 3 hr hydration, plasma ADH concentrations dropped dramatically (over 50%) to 9.2 pg/ml. No changes in plasma ADH concentrations occurred during feed restriction and refeeding. Hematocrit percentages were also determined and differences are hypothesized to relate to probable differences in environmental adaptability and genetic selection for meat or milk production among the three breeds.

Topics: Animals; Cattle; Dehydration; Drinking; Eating; Feces; Hematocrit; Kinetics; Vasopressins

To assess the role of endogenous opioids in the secretion of pituitary and adrenal hormones, we injected intravenously the antagonist naloxone (1 mg/kg) into six dogs, euhydrated or dehydrated. Plasma renin activity (PRA), osmolality, and concentrations of adrenocorticotropic hormone (ACTH), cortisol, aldosterone, vasopressin, Na+, and K+ were measured. Dehydration elevated (P less than 0.05) PRA, vasopressin, osmolality, and Na+. Thirty minutes after injection of naloxone, osmolality, Na+, K+, hematocrit, and plasma protein were not altered. Naloxone-induced elevations of ACTH (25 +/- 10 and 22 +/- 4 pg/ml) and cortisol (4.8 +/- 1.0 and 5.1 +/- 1.0 micrograms/dl) were similar during euhydration and dehydration, respectively. The increase in aldosterone due to naloxone was greater after euhydration (7.7 +/- 3 ng/dl) than during dehydration (2.3 +/- 0.8 ng/dl). Naloxone increased vasopressin by (5.3 +/- 2.8 microU/ml) during dehydration but not during euhydration. Intravenous hypertonic saline infusions showed that naloxone potentiates the osmotic release of vasopressin. Our results indicated that dehydration did not alter the inhibitory role of opioids in regulation of ACTH and cortisol but suppressed the inhibition of aldosterone secretion. Our findings also showed that opioids inhibit secretion of vasopressin during dehydration by decreased responsiveness to osmotic stimulation.

Topics: Adrenocorticotropic Hormone; Aldosterone; Animals; Dehydration; Dogs; Female; Hydrocortisone; Naloxone; Osmolar Concentration; Potassium; Rats; Renin; Sodium; Vasopressins

Potent natriuretic and spasmolytic peptides present in cardiac extracts recently have been identified. These atrial natriuretic factors (ANF) exert vascular and renal actions quite contrary to those of vasopressin (AVP). The ability of ANF to inhibit AVP secretion suggested a role for the peptides in the control of AVP release. The present studies report the measurement of ANF-like immunoreactivity within brain regions associated with the hypothalamo-neurohypophyseal tract and demonstrate significant water deprivation-induced reductions in ANF content of several structures (neural lobe, organum vasculosum lamina terminalis, suprachiasmatic and supraoptic nuclei) but not in others (median eminence, paraventricular nucleus, cortex and pituitary). The data suggest the production of ANF-like peptides within the brain and, further, the involvement of central ANF in extracellular fluid volume regulation.

Topics: Animals; Atrial Natriuretic Factor; Brain; Dehydration; Hypothalamo-Hypophyseal System; Male; Muscle Proteins; Rats; Rats, Inbred Strains; Tissue Distribution; Vasopressins; Water Deprivation

Topics: Aged; Dehydration; Euthanasia; Euthanasia, Passive; Humans; Vasopressins

Under controlled light-dark cycle (LD 12:12) and two hydratory conditions, mongrel dogs display marked day-night variations in urine flow and in its constituents. Diurnal peaks were found in urine flow and sodium excretion, while nocturnal peaks were observed in osmolality and potassium excretion. Diuretic responses, after fluid intake, were consistently faster and higher during the day than during the night. Nocturnal increases were found in plasma antidiuretic hormone (ADH), in aldosterone and in plasma renin activity (PRA), which could partially explain the present results. In all dogs there was a decrease in ADH level in the early morning hours which could account for the increased urine flow and decreased osmolality observed at this time. Plasma cortisol did not show significant temporal variations throughout the 24-hour period. Kidney denervation did not alter the day-night variations in urinary flow, sodium and osmolality, but affected the pattern of potassium excretion. A neural control of potassium excretion pattern, probably mediated by PRA-aldosterone is tentatively postulated.

Topics: Aldosterone; Angiotensins; Animals; Autonomic Nervous System; Circadian Rhythm; Dehydration; Denervation; Dogs; Female; Hormones; Hydrocortisone; Kidney; Potassium; Renin; Sodium; Urination; Vasopressins

The interaction between chlorpromazine (CPZ) and lithium on renal concentrating ability was studied in rats fed a Li-containing diet for 8 weeks (plasma-Li 0.6-0.7 mmol/l). CPZ (15 mg/kg daily orally) reduced the polydipsia and increased the ability to concentrate the urine upon water deprivation in rats treated with lithium. CPZ also reduced systolic blood pressure, but had no effect on the glomerular filtration rate or plasma levels of arginine vasopressin (AVP) in hydrated rats treated with lithium. However, CPZ prevented the rise in plasma AVP levels observed in lithium-polyuric rats in response to dehydration. During anaesthesia CPZ partially restored the impaired anti-diuretic response to exogenous AVP in rats treated with lithium. CPZ had no influence on plasma-Li levels in rats treated with lithium. It is suggested that CPZ by unknown mechanisms interferes with the effects of lithium on the water permeability response to AVP.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Chlorpromazine; Dehydration; Diabetes Insipidus; Female; Inulin; Lithium; Male; Osmolar Concentration; Rats; Rats, Inbred Strains; Vasopressins

The effects of reserpine on the osmotically induced release of pituitary vasopressin were studied (i) by measuring the urinary excretion and the vasopressin content of the neural lobe of pituitary, and (ii) by examining the ultrastructural morphology of axons in the neural lobe of dehydrated rats. After water deprivation for two days, control rats displayed characteristic antidiuretic response including a 75% reduction of urinary excretion and a six-fold decrease in vasopressin content of the neural lobe associated with a dramatic depletion of neurosecretory granules in corresponding axons. In contrast, when they received two dialy injections of reserpine, animals dehydrated for two days showed both urinary excretion and vasopressin contents in the neural lobe that remained at levels comparable to those measured in the normally hydrated rats. Additionally, neural-lobe axons of such dehydrated, reserpine-treated rats displayed a normal amount of neurosecretory granules. These data indicate that reserpine inhibits release of vasopressin from the neural lobe and favour the concept of a facilitatory role of the catecholaminergic innervation in the control of hypothalamo-neurohypophysial vasopressin-secreting neurons.

Topics: Animals; Dehydration; Male; Microscopy, Electron; Pituitary Gland, Posterior; Rats; Rats, Inbred Strains; Reserpine; Vasopressins

Immunoreactive-vasopressin, -oxytocin, -dynorphin, -dynorphin-(1-8), -alpha-neo-endorphin and -[Met]enkephalin were, in each case, present in greater concentrations in dorsal as compared to ventral, and lumbo-sacral as compared to cervico-thoracic, spinal cord. These differences were significantly more pronounced for vasopressin and oxytocin than for the other peptides. Lesions of the hypothalamic paraventricular nucleus depleted levels of immunoreactive-vasopressin and -oxytocin throughout the cord whereas levels of the opioid peptides therein were unaffected. In contrast, destruction of either the supraoptic or suprachiasmatic nucleus failed to change the content of immunoreactive-vasopressin, -oxytocin or any of the opioid peptides in the cord. Dehydration for 3 days depressed levels of immunoreactive-vasopressin, -oxytocin and -dynorphin in the neurointermediate lobe of the pituitary. In distinction, the levels of these were not modified in the spinal cord. Further, treatment with the synthetic corticosteroid, dexamethasone, elevated levels of immunoreactive-vasopressin, -oxytocin and -dynorphin in the neurointermediate pituitary whereas these were unaffected in the spinal cord. It is concluded that vasopressin and oxytocin in the spinal cord are predominantly derived from the paraventricular nucleus, localized in dorsal lumbo-sacral regions of the cord and insensitive to endocrinological manipulations. These pools may, thus, be modulated differently from their counterparts in the neurohypophysis and have a differing role, possibly in the control of the primary processing, autonomic or motor junctions. Further, there is no evidence from these or our prior studies for a close interrelationship of spinal cord vasopressin with dynorphin-related peptides (or oxytocin with [Met]enkephalin), likewise in contrast to the neurohypophysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Brain Mapping; Dehydration; Dexamethasone; Dynorphins; Endorphins; Enkephalin, Methionine; Hypothalamus; Oxytocin; Rats; Spinal Cord; Vasopressins

The regulation of sodium metabolism and the renin-angiotensin-aldosterone system was evaluated during 24 h of water, but not food, deprivation and during rehydration in the dog. Dehydration caused increases in plasma concentrations of sodium (6.0 +/- 0.7 meq/l), protein (0.8 +/- 0.1 g/dl), vasopressin (5.3 +/- 0.9 pg/ml), and renin activity (3.5 +/- 1.1 ng AI X ml-1 X 3 h-1). Plasma aldosterone was unchanged and plasma potassium fell slightly (0.2 +/- 0.1 meq/l). During dehydration, food, and thus sodium intake fell by more than 10% in 12 of 19 dogs, but urinary sodium excretion increased significantly, leading to a negative sodium balance (1.9 +/- 0.2 meq/kg). Sodium retention was observed after rehydration and sodium balance; plasma electrolytes, vasopressin, and plasma renin activity (PRA) returned turned to control levels after the 1st day of recovery. However, plasma aldosterone was slightly elevated at this time, returning to control after the 2nd day of recovery. The dehydration-induced natriuresis could not be accounted for by a fall in plasma aldosterone. However, sodium retention following rehydration could be aldosterone dependent, because additional studies showed a threefold rise in plasma levels of the hormone 1 h after drinking. The acute rise in aldosterone correlated closely (r = 0.82) with the fall in plasma sodium after drinking but not with changes in adrenocorticotrophic hormone, PRA, or plasma potassium. It is concluded that natriuresis is a homeostatic response to dehydration as a means of ameliorating the rise in body fluid osmolality.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aldosterone; Animals; Body Fluids; Body Weight; Dehydration; Dogs; Female; Homeostasis; Male; Natriuresis; Osmolar Concentration; Potassium; Renin; Renin-Angiotensin System; Sodium; Vasopressins; Water Deprivation

During exercise in the heat, sweat output often exceeds water intake, resulting in hypohydration, which is defined as a body fluid deficit. This fluid deficit is comprised of water loss from both the intracellular and extracellular fluid compartments. Hypohydration during exercise causes a greater heat storage and reduces endurance in comparison with euhydration levels. The greater heat storage is attributed to a decreased sweating rate (evaporative heat loss) as well as a decreased cutaneous blood flow (dry heat loss). These response decrements have been attributed to both plasma hyperosmolality and a plasma hypovolemia. Subject gender, acclimation state, and aerobic fitness do not alter the increased heat storage when hypohydrated. Hyperhydration, or body fluid excess, does not seem to provide a clear advantage during exercise-heat stress, but will delay the development of hypohydration.

Topics: Aldosterone; Blood Volume; Body Fluid Compartments; Body Fluids; Body Temperature Regulation; Dehydration; Drinking; Hemodynamics; Hot Temperature; Humans; Physical Exertion; Sweating; Vasopressins

Despite the absence of vasopressin, Brattleboro homozygous (DI) rats concentrate their urine to hypertonic levels when deprived of drinking water for 24 h. Glomerular filtration rate (GFR) falls concurrently and might contribute to the increased concentrating ability. The present studies concerned the time course of the changes in concentrating ability and GFR during the early hours of dehydration. Experiments were performed in 10 chronically catheterized conscious DI rats in the normally hydrated control state and during 3 h of fluid deprivation. Urine osmolality (Uosmol) increased from 97 +/- 6 (SE) to 325 +/- 11 mosmol/kg H2O at 3 h. Averaged over the 3 h, neither GFR nor effective renal blood flow changed significantly (103 +/- 2 and 106 +/- 4% of control, respectively). Fractional excretion of sodium (FENa) rose markedly from 0.3 +/- 0.1 to 1.3 +/- 0.1% at its peak. Clearly, a fall in GFR cannot explain the rise in Uosmol during the first 3 h. Plasma oxytocin (OT) increased from 5.6 +/- 0.8 to 36.4 +/- 4.5 pg/ml after 3 h of dehydration. In additional experiments, d(CH2)5-D-Phe-VAVP, an antidiuretic antagonist (anti-ADH), was administered to eight DI rats after 3-h dehydration. Control, 3-h dehydration, and post-anti-ADH values were, respectively: for Uosmol, 102 +/- 7, 347 +/- 14, 145 +/- 11 mosmol/kg H2O; for GFR, 1,003 +/- 43, 1,042 +/- 59, 866 +/- 54 microliter X min-1 X 100 g body wt-1; for FENa, 0.4 +/- 0.1, 1.4 +/- 0.1, 0.5 +/- 0.1%. The decreases following anti-ADH were all statistically significant. We conclude that OT is released during the early hours of dehydration in the DI rat and has at least three renal effects. It causes a natriuresis, it maintains renal hemodynamics and GFR during the volume contraction, and it elicits a weak antidiuretic response.

Topics: Animals; Dehydration; Diuresis; Glomerular Filtration Rate; Hemodynamics; Homozygote; Kidney; Oxytocin; Rats; Rats, Brattleboro; Rats, Mutant Strains; Regional Blood Flow; Vasopressins

Glomerular visceral epithelial cells (podocytes) undergo flattening and spreading of major processes detectable by scanning electron microscopy in early postischemic acute renal failure in both animals and man. The authors examined the kinetics of development of these epithelial cell changes in the renal pedicle-clamping model of ischemic renal failure in the rabbit. They found that these changes develop progressively, increasing with increasing length of ischemia, and occur while the pedicle clamp is still in place. To assess the possible role of angiotensin II and vasopressin in producing the epithelial changes, the authors compared glomerular morphology before and during pedicle clamping in hydrated rabbits and in dehydrated rabbits. Dehydration alone produced changes in glomerular epithelial cells comparable to those seen in the postischemic kidney. The angiotensin-converting enzyme inhibitor captopril did not prevent the podocyte changes in either group. In vitro incubation studies confirmed that both angiotensin II and vasopressin produce glomerular epithelial cell changes with a threshold between 10(-7) M and 10(-8) M, a concentration that may be physiologically significant for angiotensin II, which is synthesized at the glomerulus and may have local paracrine effects. Such local synthesis may not be inhibited by systemic administration of captopril. Angiotensin II may play a role in producing podocyte alterations during renal ischemia, as well as in the dehydrated state.

Topics: Angiotensin II; Animals; Constriction; Dehydration; Epithelium; Female; Ischemia; Kidney Glomerulus; Kinetics; Rabbits; Vasopressins

Despite the absence of vasopressin, Brattleboro homozygous (DI) rats concentrate their urine to hypertonic levels when deprived of drinking water. Ultimately this rise in urine osmolality must follow from increased osmolality of the corticopapillary gradient and/or increased osmotic equilibration across the collecting ducts. In this study we examined the concentrations and contents of total solute, urea, and nonurea solute in tissue from cortex to papillary tip of DI rats before and after dehydration for 12, 24, and 48 h. The greatest increase in osmolality occurred during the first 12 h; both urea and nonurea solute concentrations increased, but urea preferentially. From 12 to 48 h there were only small further increases in these concentrations, largely as a result of decreased tissue water content. Osmotic equilibration (reflected by urine/papillary tip osmolality) increased dramatically during dehydration, presumably because of decreased flow rate, attaining full equilibration by 48 h. The rise in urine osmolality during the first 12 h of dehydration was due to increased osmotic equilibration and to the enhanced corticopapillary gradient; urine became more concentrated from 12 to 48 h largely as a result of increased osmotic equilibration.

Topics: Animals; Dehydration; Diabetes Insipidus; Female; Kidney Concentrating Ability; Kidney Cortex; Kidney Medulla; Male; Osmolar Concentration; Rats; Rats, Brattleboro; Urea; Vasopressins

Prostaglandin (PG) production by the kidney is known to be reduced both in vivo and in vitro in rats with hereditary diabetes insipidus (DI), totally lacking ADH. Exogenous ADH restores normal PG excretion in these rats. On the other hand, osmolality in vitro, and urine flow rate in vivo have been shown to influence PG synthesis rate. In order to determine whether the decreased PG synthesis of DI rats is due to the lack of antidiuretic hormone itself or to low tissue osmolality, we studied in vivo and in vitro PG production in DI rats in which urine osmolality had been raised either with ADH (infused by Alzet minipumps), or without ADH (by dehydratation) and in control DI rats. PGE2 and PGF2 alpha were measured by radioimmunoassay in the urines and in supernatants of papillary homogenates incubated at 37 degrees C for 15-120 min. ADH administration and dehydration led to similar urine osmolalities (congruent to 900-1,000 mosmol/kg H2O versus 150 in controls). However, only ADH administration but not dehydration increased PG urinary excretion (X 5, P less than 0.001) and subsequent in vitro papillary synthesis (X 1.6, P less than 0.01). These results show that antidiuretic hormone increases PG-synthesis of the renal papilla directly and not through its effects on papillary osmolality.

Topics: Animals; Dehydration; Diabetes Insipidus; Kidney Medulla; Osmolar Concentration; Prostaglandins E; Prostaglandins F; Rats; Rats, Brattleboro; Vasopressins

It is very rare for disturbances of water balance to occur as isolated phenomena. More commonly, mixed electrolyte abnormalities present. However, to permit the logical application of therapy an understanding of basic water balance in health and disease is essential.

Topics: Dehydration; Diabetes Insipidus; Diabetes Mellitus; Humans; Osmolar Concentration; Thirst; Vasopressins; Water; Water Intoxication; Water Loss, Insensible; Water-Electrolyte Imbalance

A mathematical model of the adrenal postpituitary system has been used in cases of brain disease in which endocrine disturbances play an aggravating role. A computer simulation has suggested a type of therapy adding vasopressin to corticoids; this association seems to elicit better results than corticoids alone. Posttraumatic disorders of the cerebral hydration, on one hand, and inoperable or recurrent tumors, on the other hand, take advantage of such a systemic, formalized approach.

Topics: Adrenal Cortex Hormones; Adrenocorticotropic Hormone; Aged; Arginine Vasopressin; Astrocytoma; Brain Diseases; Brain Neoplasms; Computers; Dehydration; Dexamethasone; Drug Therapy, Combination; Humans; Hydrocortisone; Models, Theoretical; Neoplasm Recurrence, Local; Thalamus; Vasopressins

An infant with microcephaly and delayed development was found to have chronic asymptomatic hypernatremia. Computerized brain tomography disclosed dysplasia of the midline structures, septum pellucidum and corpus collosum. Evaluation revealed defective osmoregulation, hypothalamic hypothyroidism, and hypogonadotropinism. He showed no desire to drink at plasma osmolalities over 330 mOsm/kg. His plasma vasopressin levels (less than or equal to 1.4 pg/ml) were inappropriately low relative to his high levels of plasma osmolality (greater than or equal to 310 mOsm/kg), which might be accounted for by either deficient neurohypophyseal vasopressin stores or disturbance of the hypothalamic osmoreceptors governing vasopressin. The first possibility was ruled out by demonstrating normal vasopressin response (167 pg/ml) to nonosmotic (emetic) stimulation. Under baseline conditions, his urine was concentrated up to 747 mOsm/kg and urine volume was low. With water loading, maximal water diuresis developed (urine osmolality 68 mOsm/kg), but his plasma osmolality remained in the hyperosmolar range (312 mOsm/kg). Treatment with a vasopressin analogue, desamino-D-arginine vasopressin, and forced hydration restored plasma osmolality and plasma sodium to normal. These findings indicate a severe defect in the hypothalamic osmoreceptors controlling thirst and vasopressin secretion with normal vasopressin stores and preserved vasopressin responsiveness to nonosmotic stimuli. To our knowledge, this report provides the first documentation of selective osmoreceptor defect in conjunction with congenital dysplasia of midline brain structures.

Topics: Brain; Deamino Arginine Vasopressin; Dehydration; Developmental Disabilities; Humans; Hypernatremia; Infant; Male; Microcephaly; Osmolar Concentration; Thirst; Vasopressins

Topics: Adrenocorticotropic Hormone; Dehydration; Female; Humans; Hypothalamo-Hypophyseal System; Lactation; Learning; Memory; Neurophysins; Ovary; Oxytocin; Pituitary Gland, Anterior; Pregnancy; Thirst; Vasopressins

Normal Long-Evans rats, when dehydrated for up to 72 h, have a progressive rise in plasma vasopressin that is associated with a fall in body weight and urine volume, a rise in plasma and urine osmolality, and the maintenance of normal systolic blood pressure. In contrast, Brattleboro diabetes insipidus rats, genetically deficient in vasopressin, when dehydrated to achieve an equivalent body weight loss, have a significant 15 mmHg fall in systolic blood pressure. Even when fluid balance is corrected in the Brattleboro rats by the continuous administration of 1-desamino-8-D-arginine vasopressin, a synthetic vasopressin analogue with potent antidiuretic properties but minimal pressor activity, blood pressure still falls when the animals are dehydrated. In contrast, Brattleboro rats infused with exogenous arginine vasopressin to produce a plasma vasopressin level of 18.9 +/- 3.5 pg X ml-1 are able to maintain normal blood pressure during 48 h of dehydration. This level of vasopressin is comparable to the level found endogenously in dehydrated Long-Evans rats and is nonpressor in normal rats. These results suggest that both the antidiuretic and vasoconstrictor properties of vasopressin are important in the cardiovascular response to dehydration.

Topics: Angiotensin II; Animals; Arginine Vasopressin; Blood Pressure; Deamino Arginine Vasopressin; Dehydration; Electrolytes; Female; Kidney; Osmolar Concentration; Pituitary Gland, Posterior; Rats; Rats, Brattleboro; Renin; Urine; Vasopressins

Plasma vasopressin concentrations (pAVP) are elevated during dehydration due to alterations in extracellular fluid (ECF) volume and tonicity. The contributions of the reduction in volume and increase in plasma osmolality to the rise in pAVP were assessed in 6 dogs with bilateral carotid loops following 24 h of fluid, but not food, deprivation. Dehydration significantly (p less than 0.05) increased plasma osmolality from 297 +/- 1 to 315 +/- 2 mosm/kg), decreased body weight from 20.8 +/- 1.2 to 20.3 +/- 1.2 kg, and elevated pAVP from 1.4 +/- 0.2 to 5.3 +/- 0.6 pg/ml. The effect of extracellular fluid volume reduction was tested by reexpanding this compartment in dehydrated dogs with 0.15 M NaCl. Plasma vasopressin concentration was significantly reduced by 1.3 +/- 0.2 pg/ml (33 +/- 4%) and plasma osmolality unchanged following volume replacement. The contribution of the increase in plasma osmolality was assessed by bilateral intracarotid infusions of water at 0.6 ml/min/artery which lowered jugular venous plasma osmolality to euhydrated values (296 +/- 4 mosm/kg), but did not significantly reduce systemic plasma osmolality. Plasma vasopressin levels were significantly reduced 3.2 +/- 1.1 pg/ml (70 +/- 5%). Thus, following 24 h of fluid deprivation in dogs, the rise in pAVP is due to changes in both ECF volume and tonicity. The increase in tonicity plays a greater role in the elevation of pAVP, than the reduction in volume.

Topics: Animals; Blood Volume; Dehydration; Dogs; Extracellular Space; Osmolar Concentration; Renin; Vasopressins

The effect on body temperature (Tb) regulation of alterations in the osmotic milieu of the intracranial compartment has been examined by intracerebroventricular (ICV) infusion of water (0.034 ml . min-1) in heat-stressed hydrated and dehydrated cats. At an ambient temperature (Ta) of 38 degrees C, before ICV water infusion, mean Tb (measured in the hypothalamus) of normally hydrated cats was 38.8 +/- 0.1 degree C and mean evaporative water loss (EWL) was 1.32 +/- 0.18 W . kg-1. ICV water infusion was without significant effect (P greater than 0.05, t-test) on either of these values in normally hydrated animals. In dehydrated animals at Ta 38 degrees C, Tb and EWL were both significantly altered (P less than 0.001) from the normally hydrated state and were measured at 39.9 +/- 0.2 degree C and 0.84 +/- 0.09 W . kg-1 respectively. Infusion of water into dehydrated animals significantly altered pre-infusion levels of Tb and EWL so that Tb fell to 39.4 +/- 0.2 degree C (P less than 0.001) and EWL rose to 1.46 +/- 0.09 W . kg-1 (P less than 0.001). No effect of ICV water infusion on mean plasma vasopressin levels (pAVP) was observed in normally hydrated animals (preinfusion pAVP = 1.3 +/- 0.2 microunit . ml-1, post-infusion pAVP equal 1.3 +/- 0.3 microunit . ml-1, P greater than 0.05). However, a significant reduction in pAVP occurred subsequent to infusion in dehydrated animals (pre-infusion pAVP equal 16.6 +/- 1.85 microunits . ml-1, post-infusion pAVP equal 10.7 +/- 2.3 microunits . ml-1, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Body Temperature Regulation; Brain; Cats; Dehydration; Female; Hot Temperature; Male; Osmolar Concentration; Stress, Physiological; Vasopressins; Water Loss, Insensible; Water-Electrolyte Balance

Despite the absence of vasopressin, Brattleboro homozygous (DI) rats can concentrate their urine to hypertonic levels when deprived of drinking water. When DI rats are infused with vasopressin, freeze-fracture electron microscopy has revealed increases in intramembranous particle clusters (IPC) in papillary collecting duct luminal membrane that parallel the rise in urine osmolality. In the present study, we examined whether the increase in concentrating ability of DI rats dehydrated for 24 h was associated with a change in IPC. For comparison, oral water loading and 24-hour dehydration were used to suppress and stimulate endogenous vasopressin secretion in Long-Evans (LE) rats, and the effects on urine osmolality and IPC were examined. In LE rats, the induced changes in water balance resulted in alterations in IPC frequency that paralleled urine osmolality, whereas, in DI rats, frequency of IPC remained low under all conditions, even when urine osmolality rose to almost 1,000 mosm/kg H2O as a result of 24-hour dehydration. These results suggest that the increased concentrating ability of dehydrated DI does not depend upon increased water permeability of the papillary collecting ducts.

Topics: Animals; Dehydration; Freeze Fracturing; Kidney Concentrating Ability; Kidney Tubules; Kidney Tubules, Collecting; Rats; Rats, Brattleboro; Vasopressins; Water-Electrolyte Imbalance

Uncertainty exists as to whether endogenous angiotensin activates brain mechanisms controlling vasopressin (AVP) secretion during dehydration. We injected various doses of saralasin into a lateral cerebroventricle (IVT) of conscious, male rats deprived of water for 48 h and killed them at different times. The concentration of AVP in the plasma (p[AVP]), measured by radioimmunoassay, was unaffected by saralasin. IVT pretreatment with 1-Sar-8-Ile-angiotensin II blocked maximal AVP release by IVT angiotensin, but this pretreatment did not reduce p[AVP] after 24, 48 or 72 h water deprivation. A 3-hour continuous IVT infusion of CSF or saralasin (10 micrograms/h) into 48-hour water-deprived rats revealed equivalent p[AVP] and urine volumes. When the infusions were continued for 3 h more with water available, control and saralasin-treated rats: (a) drank at similar rates, (b) excreted similar amounts of urine, and (c) reduced their p[AVP] levels to the same extent. IVT saralasin did not affect p[AVP] of rats dehydrated with hypertonic NaCl. Combined IVT saralasin and atropine reduced p[AVP] of 48-hour water deprived rats about 30% (p less than 0.05). We conclude that redundancy exists for sensing, integrating and releasing vasopressin in dehydrated rats.

Topics: 1-Sarcosine-8-Isoleucine Angiotensin II; Animals; Atropine; Dehydration; Drinking Behavior; Injections, Intraventricular; Male; Radioimmunoassay; Rats; Rats, Inbred Strains; Saline Solution, Hypertonic; Saralasin; Vasopressins; Water Deprivation

Magnocellular neurons in the supraoptic and paraventricular nuclei synthesize and release vasopressin and oxytocin in response to dehydration. Pinealectomy has been observed to decrease the distribution in the supraoptic nuclei of thiamine diphosphate-phosphohydrolase, an enzyme specific for the Golgi apparatus that correlates positively with neurosecretory activity. Based upon these studies we postulated that pinealectomy would alter the concentration of neurohypohysial hormones in plasma elevated by 48 hr of water deprivation. In addition, we investigated the possibility that pinealectomy would affect vasopressin concentration in another circumventricular organ, the subfornical organ (SFO) and in a adjacent fiber tract of the limbic system, the hippocampal commissure-fornix (HC-F). Adult, male, Sprague-Dawley rats exposed to a 12 hr light/dark cycle were either unoperated (controls; C), sham-operated (Sham; S) or pinealectomized (PX) three weeks prior to testing. Food and water consumption and urinary excretion of Na and K were measured for 7 days. On the fifth day, half of the animals in each treatment group (C, S, PX) were deprived of water for 48 hr. Animals were decapitated on day 8. Vasopressin and oxytocin in plasma were extracted using bentonite and acetone-ether, respectively, then quantified by radioimmunoassay. The SFO and HC-F were microdissected from each brain. Like tissues from 4 rats were pooled, homogenized in 0.1 N HCl, and centrifuged. The supernatant was neutralized and vasopressin was quantified by radioimmunoassay. Dehydration resulted in antidiuresis, increased urine concentrations of Na and K, a decreased ratio of Na:K in urine, and reduced food consumption of similar magnitudes in all groups (C, S, PX; p greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Body Weight; Dehydration; Eating; Hematocrit; Hippocampus; Light; Male; Neurosecretory Systems; Oxytocin; Pineal Gland; Rats; Rats, Inbred Strains; Subfornical Organ; Time Factors; Vasopressins

Mildly dehydrated conscious Merino ewes were infused with vasopressin (AVP) at 5 mu x min-1 alone and simultaneously with the angiotensin II receptor blocker sar1ala8-angiotensin II (saralasin) at 15 micrograms x min-1. AVP was slightly pressor and produced an increase in the calculated total peripheral resistance, and an increase in glomerular filtration rate, urine flow and electrolyte excretion, without a change in total renal plasma flow. These results indicate renal efferent arteriolar vasoconstriction as well as other non-renal vasoconstriction. Saralasin infusion checked the rise in total peripheral resistance (which continued to increase after saralasin withdrawal), but caused a marked increase in renal vascular resistance resulting in a decrease in renal plasma flow and to a lesser extent in glomerular filtration rate. These results suggest that saralasin was acting as an angiotensin II agonist in the kidney, but as an antagonist elsewhere. Deductions from previous experiments in the literature of the renal function of angiotensin II, based on its supposed inhibition by saralasin, may not be justified.

Topics: Angiotensin II; Animals; Dehydration; Female; Kidney; Saralasin; Sheep; Vasopressins

Topics: Animals; Dehydration; Diabetes Insipidus; Glucagon; Insulin; Male; Neurotensin; Peptides; Pituitary Gland, Anterior; Pituitary Gland, Posterior; Rats; Rats, Brattleboro; Rats, Mutant Strains; Somatostatin; Substance P; Vasopressins

Topics: Aging; Animals; Dehydration; Diabetes Insipidus; Heterozygote; Male; Models, Biological; Pituitary Gland, Posterior; Rats; Rats, Brattleboro; Rats, Inbred F344; Rats, Mutant Strains; Vasopressins; Water Deprivation

Topics: Animals; Carboxy-Lyases; Deamino Arginine Vasopressin; Dehydration; Diabetes Insipidus; Hepatectomy; Kidney; Ornithine Decarboxylase; Polyamines; Rats; Rats, Brattleboro; Rats, Mutant Strains; Testosterone; Vasopressins

Topics: Animals; Consciousness; Dehydration; Drinking; Male; Potassium; Rabbits; Renin; Sodium; Vasopressins; Water Deprivation

Topics: Adolescent; Adult; Aged; Dehydration; Diabetes Insipidus; Female; Humans; Male; Middle Aged; Osmotic Pressure; Vasopressins

The relation between plasma osmolality (pOsm) and the concentration of immunoreactive vasopressin in plasma from an external jugular vein (pAVP) was studied in dogs prepared with carotid loops and anesthetized with chloralose-pentobarbital. Control mean pAVP was 0.6-1.0 microM/ml, after 24 h of dehydration pAVP was tripled. Isosmotic volume expansion for 10 min elicited a decrease in pAVP in all cases not associated with low control values of pAVP. I.v. hyperosmotic infusions (delta pOsm: 9 or 18 mOsm/kg in 10 min) increased pAVP. No significant alterations in pAVP occurred in relation to infusions during which the head or the remainder of the body was selectively supplied by hyperosmotic blood. Statistically, the distribution of the pAVP values suggests the existence of two populations, in euhydrated animals high concentrations (greater than 8 microU/ml) were found in a small fraction of the samples. It is concluded that (i) in chloralose-anesthetized, non-traumatized dogs pAVP is very similar to values found in venous plasma from conscious dogs, (ii) the pAVP measurements support the concept of an episodic secretion of vasopressin, and (iii) under the present circumstances, an ubiquitous increase in pOsm is a more effective stimulus for vasopressin release than a similar but selective increase in the osmolality of the blood flowing towards the head.

Topics: Animals; Dehydration; Dogs; Female; Osmolar Concentration; Saline Solution, Hypertonic; Sodium Chloride; Vasopressins; Water

To better understand the role of arginine vasopressin in cardiovascular regulation, we measured in unanesthetized dogs regional blood flows with radioactive microspheres before and during 1-h vasopressin infusions that increased the vasopressin concentration of plasma by 11 +/- 0.6 pg/ml. Cardiac output measured by an electromagnetic flowmeter decreased by 13%. Blood flows to the skeletal muscle and skin, the areas most affected, decreased by 30.8 and 34.3%, respectively. In the same group of dogs a period of 48-h water restriction increased plasma vasopressin by 6.9 +/- 1.3 pg/ml and reduced cardiac output by 14.4%. Skeletal muscle blood flow decreased by 32.8%, a pattern strikingly similar to that following vasopressin infusion. Obvious differences between vasopressin infusion and dehydration were also noted, in particular in the skin and splanchnic areas. However, the possibility that vasopressin contributed to the cardiovascular adjustments to dehydration must be considered. The use of an antagonist of the vascular effects of vasopressin, [1-deaminopenicillamine, 2-(O-methyl)tyrosine]arginine-vasopressin ([dPTyr(Me)]AVP), did not permit us to clarify this issue, because this analogue given alone exerted pronounced systemic and regional cardiovascular effects that resembled those of vasopressin.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Cardiac Output; Dehydration; Dogs; Male; Microspheres; Organ Specificity; Regional Blood Flow; Thirst; Vascular Resistance; Vasopressins

Topics: Animals; Dehydration; Drinking; Hypertonic Solutions; Isotonic Solutions; Macaca mulatta; Neurosecretory Systems; Osmolar Concentration; Supraoptic Nucleus; Vasopressins

Topics: Anesthesia; Animals; Brain; Creatinine; Dehydration; Diuresis; Dogs; Female; Osmolar Concentration; Saline Solution, Hypertonic; Sodium Chloride; Vasopressins; Water-Electrolyte Balance

Plasma renin activity (PRA) was measured in conscious Brattleboro strain, vasopressin (AVP)-deficient diabetes insipidus (DI) and heterozygous rats with the aid of chronically implanted catheters. Baseline, dehydration-stimulated, and hemorrhage-stimulated levels of PRA were elevated in DI rats, as compared to levels in heterozygous controls. Replacement therapy with either AVP or the nonpressor AVP analog dDAVP reduced PRA to control levels. The high level of PRA in DI rats was associated with the lack of endogenous antidiuretic activity per se and not the pressor activity associated with the vasopressin molecule. Thus, elevated PRA in the chronic absence of AVP (in DI rats) most probably results indirectly from the chronically reduced plasma volume reported associated with hypothalamic diabetes insipidus.

Topics: Animals; Consciousness; Dehydration; Hemorrhage; Rats; Rats, Brattleboro; Rats, Mutant Strains; Renin-Angiotensin System; Vasopressins

The levels of dynorphin-(1-13), leucine enkephalin, beta-endorphin and vasopressin immunoreactivity (ir-DYN, ir-1-ENK, ir-beta-END, ir-VP) have been determined in the anterior and in the neurointermediate lobes of the pituitary of rats subjected to a variety of manipulations. Dehydration of rats by 5 days enforced inhibition of a 2% solution of NaCl resulted in a significant decrease in the levels of ir-DYN, ir-1-ENK and ir-VP, but not in those of ir-beta-END in the neurointermediate lobe of the pituitary. In contrast, substitution of drinking water by a solution containing 20 microgram/ml dexamethasone for 5 days produced a significant increase in the neurointermediate pituitary content of ir-DYN, ir-1-ENK and ir-VP, whereas levels of ir-beta-END remained unaffected. This treatment, however, resulted in a significant fall in the ir-beta-END content of the adenopituitary without changing levels of ir-DYN in this structure. Adrenalectomy was associated with a significant decrease in the ir-DYN, ir-VP and ir-1-ENK content of the neurointermediate lobe of the pituitary and a pronounced elevation in the ir-beta-END but not ir-DYN content of the adenohypophysis. These observations are indicative that the regulation mechanisms of the functional state of particular endorphins differ between the anterior and neurointermediate lobes of the pituitary. The concomitant alterations in levels of ir-DYN, ir-1-ENK and ir-VP detected suggest that a common or similar mechanism of regulation may exist for these peptides. A common biosynthetic origin, however, appears to be unlikely, since Brattleboro rats which are unable to synthesize vasopressin possess unchanged ir-DYN- and ir-1-ENK- levels in the pituitary.

Topics: Adrenalectomy; Animals; beta-Endorphin; Dehydration; Dexamethasone; Diabetes Insipidus; Dynorphins; Endorphins; Enkephalin, Leucine; Enkephalins; Male; Peptide Fragments; Pituitary Gland; Rats; Rats, Inbred Strains; Sodium Chloride; Vasopressins

Abnormalities in neurohypophyseal function have been postulated to contribute to the alterations in fluid and electrolyte balance observed during aging. In this study, parameters of fluid and electrolyte balance were evaluated during chronic water deprivation in old (30 months) and young (3 months) Fischer 344 rats. The increase in serum vasopressin (VP) and renin concentrations observed in the 3 month animals following chronic water deprivation were absent in the aged rats (p less than 0.05 and p less than 0.02, respectively). This occurred in spite of apparently comparable alterations in fluid volume and osmolality (assessed by changes in body weight, hematocrit and plasma osmolality). Relative to body weight, VP content of the neural lobe was significantly reduced and was more severely depleted by dehydration in aged rats than in young rats. Thus, inadequate neurohypophyseal hormone stores may contribute to the inability of the aged animals to attain elevated serum VP concentrations during chronic stimulation. Several parameters of renal function were examined in the aged rats. Although none of the old rats were in renal failure, they all showed some indication of reduced renal function. In spite of renal abnormalities including reduced concentrating capabilities, the old rats did demonstrate a significant antidiuretic response to dehydration. However, with prolonged fluid deprivation, they were unable to attain serum VP or renin concentrations comparable to that achieved by the young rats.

Topics: Animals; Dehydration; Hypothalamo-Hypophyseal System; Kidney; Kinetics; Male; Rats; Rats, Inbred F344; Renin; Vasopressins

To evaluate the relationship of renal prostaglandin synthesis to urine-concentrating mechanisms, 14 healthy subjects received antidiuretic hormone (ADH) and the nonpressor ADH analog desamino-d-arginine vasopressin (dD'AVP). Endogenous ADH was increased by water deprivation. Urinary prostaglandin E2 (PGE2) was measured by RIA and by bioassay. ADH, dD'AVP, and dehydration each reduced urinary volume by a similar amount (from 582 +/- 66 to an average of 141 +/- 13 ml/4 h) and similarly increased osmolality (from 231 +/- 13 to 721 +/- 31 mosmol/kg). Dehydration and dD'AVP reduced PGE2 from 44 +/- 4 to 25 +/- 5 and 30 +/- 5 ng/4 h, respectively (P less than 0.01), suggesting an inverse correlation of PGE2 with urine osmolality (r = -0.48; P less than 0.005). In contrast, ADH increased urinary PGE2 to 102 +/- 23 ng/4 h (P less than 0.02). Infusions of another vasoconstrictor peptide, angiotensin II, to six of the subjects doubled urine osmolality and also increased urinary PGE2 excretion. These data do not support the theory that the antidiuretic effect of ADH enhances PG synthesis; instead, the data indicate that ADH has two effects on PGE2 excretion: 1) stimulation, presumably by pharmacological pressor activity, and 2) inhibition by antidiuresis.

Topics: Adolescent; Adult; Arginine Vasopressin; Creatinine; Deamino Arginine Vasopressin; Dehydration; Female; Humans; Male; Middle Aged; Osmolar Concentration; Potassium; Prostaglandins E; Urine; Vasopressins

Topics: Animals; Dehydration; Drinking; Dynorphins; Endorphins; Male; Pituitary Gland, Posterior; Rats; Sodium Chloride; Vasopressins

The effects of alterations of plasma osmolality on plasma arginine vasopressin (AVP) and renin activity (PRA) following graded hemorrhage were studied in conscious dogs who were either euhydrated, dehydrated, water loaded, or infused with hypertonic saline. Base-line plasma osmolality and AVP were significantly different in the four treatment groups; however, following hemorrhage the increases in log AVP did not significantly differ. An unexpected finding was that water loading resulted in significant elevations in PRA and plasma aldosterone concentrations, whereas plasma osmolality and AVP were reduced. Prior to hemorrhage, PRA was significantly greater in the water-loaded and dehydrated groups than in the euhydrated or saline-infused groups; following hemorrhage the increases in log PRA were not significantly different in all four treatment groups. The data suggest that, although alterations in osmolality influence base-line levels of AVP, they have no effect on relative (logarithmic) rises in AVP following hemorrhage. Similarly, alterations in AVP may influence base-line PRA, but do not influence relative rises in PRA following hemorrhage.

Topics: Animals; Blood Physiological Phenomena; Blood Pressure; Dehydration; Dogs; Hemorrhage; Kidney; Male; Osmolar Concentration; Renin; Vasopressins

Hyperosmolar diabetic coma is characterised by extreme hyperglycaemia and dehydration. Hypernatremia often contributes additionally to plasma hyperosmolarity. The pathogenesis of these component abnormalities is considered. The explanation of the absence of hyperketonaemia is examined in the light of recent experimental and clinical data. At the beginning of the development of the syndrome, high peripheral plasma insulin probably explains the lack of ketosis via inhibition of lipolysis. Later, when hyperosmolar coma is established, peripheral insulinopenia but an "insulinised" liver may coexist. This would favour metabolism of free fatty acids along nonketogenic pathways.

Topics: Blood; Dehydration; Diabetic Coma; Glucagon; Humans; Hyperglycemia; Hyperglycemic Hyperosmolar Nonketotic Coma; Insulin; Kinetics; Osmolar Concentration; Sodium; Uremia; Vasopressins

Topics: Aldosterone; Animals; Blood Pressure; Dehydration; Kidney; Renin; Sheep; Sodium; Urine; Vasopressins

Both dehydration to 87% of original body weight (Wo) and arginine vasotocin (AVT: 20 mU/g) elicited rapid weight gains (ca. 9% of Wo in the 1st h) when terrestrial-phase T. torosa were given access to water. In each case, net weight gain resulted from increased integumental osmosis and antidiuresis. Mesotocin (0.001 -- 0.1 micrograms/g) elicited modest but significant weight gains (ca. 1%/h) caused solely by increased integumental osmosis. Integumental water uptake from wet moss was 66% that of totally immersed animals. Water movement from ventral to dorsal body surface occurred along channels on the skin. Urinary bladder storage capacities in excess of 50% of Wo were observed. Following AVT administration, bladder water resorption increased significantly, while glomerular filtration rate dropped to 16% of control values. The structural and physiological adaptations for water balance in T. torosa are comparable to those found in some terrestrial anurans.

Topics: Animals; Body Water; Body Weight; Dehydration; Glomerular Filtration Rate; Kidney; Prolactin; Salamandridae; Urinary Bladder; Urodela; Vasopressins; Water-Electrolyte Balance

The effect of heat (35 degrees C) and dehydration under heat (30 h) on plasma levels of antidiuretic hormone (ADH) and aldosterone was studied on four nonpregnant dry Holstein cows. Heat exposure caused a rapid significant rise in plasma ADH without significant changes in hematocrit (Hct), small but significant increase in urine output and a significant reduction in total plasma protein. Dehydration under heat caused a sharp increase in ADH levels associated with a significant decrease in urine output and a significant increase in plasma protein, blood Hct, and serum osmolality. A significant reduction in plasma aldosterone level was observed after 24 h of heat exposure. This was associated with a slight rise in urinary sodium excretion and a significant reduction in serum sodium. Both serum and urinary potassium concentrations were significantly lower under heat. Dehydration resulted in a slow rise in aldosterone but did not reach thermoneutral level. This is probably due to the inhibitory effect of higher serum sodium observed during dehydration on plasma aldosterone secretion. The rise in ADH and decrease in aldosterone during heat exposure may explain why cattle are one of the few species that do not concentrate urine during heat exposure.

Topics: Aldosterone; Animals; Blood Physiological Phenomena; Blood Proteins; Body Water; Cattle; Dehydration; Female; Hot Temperature; Osmolar Concentration; Potassium; Sodium; Vasopressins

Rats dehydrated up to 12 days were given intraperitoneally propranolol hydrochloride in daily dose of 1.0 mg/100 g of initial body weight. In not dehydrated animals the only dose of propranolol increased significantly the vasopressin and oxytocin release from the neurohypophysis. In dehydrated animals propranolol restrained somewhat the decrease of vasopressin in the neurohypophysis, but intensified the vasopressin depletion in the hypothalamus. The oxytocic potency of both the neurohypophysis and hypothalamus decreased progressively in animals deprived of water. Propranolol potentiated this effect of osmoreceptor stimulation.

Topics: Animals; Dehydration; Hypothalamus; Male; Oxytocin; Pituitary Gland, Posterior; Propranolol; Rats; Vasopressins; Water Deprivation

A radioimmunoassay of ADH has been applied to the study of plasma ADH levels in various conditions. The validity of the assay has been evaluated by the usual quality control parameters of RIA and by the measure of plasma levels in 12 upright water deprived normal volunteers (mean 9.5 pg/ml, SEM +/- 1.5) in 8 resting and hydrated normal volunteers (1.3 +/- 0.4 pg/ml), in a case of diabetes insipidus (1.6 pg/ml), in 8 cases of SIADH Syndrome (range 13-77 pg/ml) and in 4 anesthetized dogs before (33.7 +/- 9.2 pg/ml) and after acute haemorrhage (66 +/- 9.5 pg/ml, p less than 0.02). The osmotoic challenge to ADH secretion has been studied in 8 patients with no overt endocrine pathology by salt perfusion and showed a significant rise (p less than 0.05) of plasma ADH from 6.3 +/- 3.1 pg/ml before, to 20.6 +/- 7.9 pg/ml during salt infusion corresponding to the significant (p less than 0.0001) rise of plasma osmolality from 273 +/- 2.8 to 288.2 +/- 1.1 m Osm/kg.

Topics: Animals; Dehydration; Diabetes Insipidus; Dogs; Hemorrhage; Humans; Inappropriate ADH Syndrome; Osmolar Concentration; Radioimmunoassay; Saline Solution, Hypertonic; Vasopressins

The relationship between plasma osmolality (pOsm) and plasma vasopressin (pAVP) was studied in 13 human subjects during dehydration. The fit of linear, log-linear, parabolic, and exponential models was tested. For all of the data, the nonlinear models had the best fit. However, when individual differences in either gain or threshold were allowed for, the linear models were better than log-linear models. Finally, analyses were made with individual data points. Linear models had the best fit in half of the subjects, whereas for the others the parabolic model gave the best fit. For those subjects investigated in the low range of the osmoregulatory curve, a linear relationship was found, whereas, for those having the most pronounced increase in pOsm, the most significant improvement was found with the parabolic model. This finding indicates that the relationship is not stable during dehydration in the whole range and that hypovolemia probably can influence the secretion rate and/or metabolic clearance rate and thereby the relationship.

Topics: Adolescent; Adult; Dehydration; Female; Humans; Male; Middle Aged; Osmolar Concentration; Plasma; Radioimmunoassay; Sodium; Vasopressins

The effects of intraventricular injection of Sar1-Ala8-angiotensin II (A specific antagonist of angiotensin II) on the plasma vasopressin level increased by intraventricular injection of angiotensin II and by water deprivation (46 h) were examined in conscious male rats with an indwelling cannula in the third cerebral ventricle. Blood samplings were made by decapitation and the plasma level of vasopressin was determined by radioimmunoassay. Twenty-five, 50 or 100 ng of angiotensin II produced significant (P less than 0.05) increase in plasma vasopressin level 90 sec after the injection. The effect of 50 ng of angiotensin II was inhibited significantly (P less than 0.05) at least with 100 ng of Sar1-Ala8-angiotensin II given 2 min before the injection of angiotensin II. The dehydrated rats to which 1000 ng of Sar1-Ala8-angiotensin II was given 5 min before the decapitation showed the significantly (P less than 0.05) lower median plasma vasopressin level than that of the dehydrated controls. No significant difference in plasma osmolality was noted between them. These results suggest that the plasma vasopressin response to intraventricular angiotensin II is produced via angiotensin II receptors in the brain and that Sar1-Ala8-angiotensin II inhibits the effect of endogenous angiotensin II on plasma vasopressin level under dehydration.

Topics: Angiotensin II; Animals; Dehydration; Injections, Intraventricular; Male; Rats; Saralasin; Vasopressins

The activated hypothalamic magnocellular neurosecretory system of the rat was studied in tissue sections, double stained with the unlabeled antibody peroxidase-antiperoxidase complex (PAP) technique. The results indicate that in animals with an activated hypothalamic magnocellular neuroendocrine system, as well as in normal animals, vasopressin and oxytocin are exclusively synthesized in separate vasopressinergic and oxytocinergic neurons.

Topics: Animals; Dehydration; Diethylstilbestrol; Histocytochemistry; Hypothalamus; Immunoenzyme Techniques; Oxytocin; Rats; Stress, Physiological; Vasopressins

Topics: Adolescent; Child; Child, Preschool; Dehydration; Diagnosis, Differential; Humans; Infant; Infant, Newborn; Metabolic Diseases; Polyuria; Urine; Vasopressins

We have studied an infant (female) with a persisting hypernatremia and adipsia, examined for the first time at the age of five months. The funtional test carried out showed an insensibility of the osmoreceptors for very important changes in POsm. carryng with them a lack of response of the ADH. Neuroradiological studies demostrated hydrocephalia secondary to a stenosis of the aqueduct of Silvio. Treatment with chlorpropamide proved effective. The literature is being revised comparing out results with those of other authors.

Topics: Chlorpropamide; Dehydration; Diuresis; Female; Humans; Hydrocephalus; Hypernatremia; Hypothalamo-Hypophyseal System; Infant; Osmolar Concentration; Radiography; Saline Solution, Hypertonic; Vasopressins; Water-Electrolyte Balance

Ethanol induced negative water balance has been previously inferred from fluid turnover rates upon initial exposure followed by restored normal fluid balance with prolonged exposure. The first two experiments of the present investigation noted hypovolemia and carcass dehydration during the initial few days of forced choice maintenance on 10% ethanol with recovery to near normal levels of intravascular volume and carcass water after 2 months of forced consumption. A third experiment attempted to test whether the alcohol induced dehydration could be corrected with the administration of exogenous ADH.

Topics: Alcohol Drinking; Animals; Body Water; Dehydration; Drinking Behavior; Ethanol; Male; Rats; Time Factors; Vasopressins

Topics: Animals; Arginine Vasopressin; Dehydration; Hypothalamus; Hypothalamus, Middle; Male; Median Eminence; Nerve Fibers; Paraventricular Hypothalamic Nucleus; Pituitary Gland, Posterior; Radioimmunoassay; Rats; Supraoptic Nucleus; Vasopressins

Despite the apparent absence of vasopressin (ADH), Brattleboro homozygotes [diabetes insipidus (DI) rats] can concentrate their urine when deprived of drinking water. Since other investigators have shown that reducing glomerular filtration rate (GFR) improves the concentrating ability of water-loaded dogs, the present studies were undertaken to quantify the magnitude and time course of changes in GFR during dehydration. Clearance experiments were performed in 10 conscious DI rats before and following 3, 6, 9, 12, 15, and 24 h of dehydration. Urine osmolality increased from 155.0 +/- 12.6 (SE) to 696.7 +/- 8.4 mosmol/kg H2O after 24 h. GFR averaged 984.3 +/- 79.6 microliters . min-1 . 100 g body wt-1 in the control phase, fell to about 80% of this value over the first 12 h of dehydration, and then declined to 27% at 24 h. The rats lost 20% of their body weight over the 24 h. The osmolality of the papillary tip averaged 896 +/- 44 mosmol/kg H2O at 24 h compared to a control value of 493 +/- 28. The lack of osmotic equilibration between urine and papillary interstitium suggests that dehydration did not appreciably increase the water permeability of the distal nephron. These experiments clearly show a progressive decline in GFR as urine becomes concentrated during dehydration in the absence of ADH; these events may or may not be causally related.

Topics: Animals; Dehydration; Diabetes Insipidus; Female; Glomerular Filtration Rate; Kidney Concentrating Ability; Kidney Medulla; Male; Osmolar Concentration; Rats; Urine; Vasopressins

Topics: Adolescent; Arginine Vasopressin; Dehydration; Diabetes Insipidus; Diagnosis, Differential; Eosinophilic Granuloma; Female; Humans; Hypothalamo-Hypophyseal System; Osmolar Concentration; Recurrence; Vasopressins

Topics: Adult; Arginine Vasopressin; Dehydration; Female; Humans; Male; Middle Aged; Radioimmunoassay; Reference Values; Vasopressins

Examination of the toad urinary bladder by freeze-fracture electron microscopy reveals intramembrane particle arrays at a number of membrane sites. An array in which particles are aggregated into closely apposed parallel rows is found in the granular cell luminal membrane of dehydrated toads fixed in situ. These aggregates are structurally indistinguishable from those previously associated with vasopressin exposure in vitro. Aggregates are not found in granular cell luminal membrane in the case of hydrated toads fixed in situ. However, structurally similar arrays are found at low frequency in the membrane of cytoplasmic vacuoles in granular cells and in the plasma membrane of basal cells in both hydrated and dehydrated toads. Aggregates are also present at these sites in control and vasopressin-treated bladders from in vitro experiments. Particle arrays characteristic of gap junctions, desmosomes and hemidesmosomes also occur in the plasma membrane of basal cells. In addition, distinctive square arrays of particles exist in the plasma membrane of the bladder's mesothelium. Although a variety of intramembrane particle arrays exist in the toad urinary bladder, only the occurrence of organized particle aggregates in the luminal membrane of granular cells appears to be associated with vasopressin exposure.

Topics: Animals; Bufo marinus; Cell Membrane; Dehydration; Epithelium; Female; Freeze Fracturing; Granulocytes; Microscopy, Electron; Urinary Bladder; Vasopressins

In rats dehydrated up to 12 days the neurohypophysial vasopressin content was determined by Dekański's method. Carbamylcholine inhibited somewhat the vasopressin depletion in the neurohypophysis, but not earlier than under severe dehydration (8th and 12th day). A single dose of atropine given 24 h prior to sacrifice to not dehydrated animals resulted in a diminution of the vasopressin content in the neurohypophysis; in animals dehydrated for four days and parallely atropinized the decrease of the neurohypophyseal vasopressin content was, on the contrary, considerably inhibited. Under severe dehydration, the treatment with atropine did not change the vasopressin stores in the neural lobe. Phenoxybenzamine inhibited the vasopressin depletion in the neural lobe following four days of dehydration. Under severe dehydration, amphetamine potentiated the effect of osmoreceptor stimulation. It is supposed that impulses of osmoreceptor origin are of some importance in determining the vasopressin release following changes of cholinergic or adrenergic transmission.

Topics: Amphetamine; Animals; Atropine; Carbachol; Dehydration; Male; Phenoxybenzamine; Pituitary Gland, Posterior; Rats; Synaptic Transmission; Vasopressins

1. The role of vasopressin in blood pressure control and in the pathogenesis of one-kidney Goldblatt hypertension in the conscious dog was investigated. 2. Infusion of synthetic arginine vasopressin to elevate plasma levels approximately five-fold caused bradycardia in normal dogs and increase in mean arterial blood pressure in dogs with pharmacological autonomic blockade. 3. A similar degree of elevation of plasma vasopressin concentration was observed after mild non-hypotensive haemorrhage. 4. Renal artery constriction in unilaterally-nephrectomized dogs caused a rise in plasma renin activity and only a doubling of plasma vasopressin concentration, but a marked rise in mean arterial blood pressure. 5. Vasopressin may play a role in normal cardiovascular homeostatic responses, but its role in the pathogenesis of this form of hypertension is unlikely to be significant.

Topics: Animals; Autonomic Nervous System; Blood Pressure; Dehydration; Dogs; Hemorrhage; Hypertension, Renal; Hypertension, Renovascular; Male; Vasopressins

The subfornical organ (SFO), a neuroendocrine structure implicated in saltwater homeostasis, contains secretory structures histochemically similar to those in the neurohypophysis. Because of these morphological similarities, we compared levels of vasopressin (vp) in the SFO area and the adjacent hippocampal commissure-fornix (HC-F) of normally hydrated and 48 h water-deprived (WD) rats. VP in the SFO region from normally hydrated rats was 44 +/- 5 pg/mg protein, 3.5 +/- 0.4 ng/g wet weight or 3.6 +/- 0.4 pg/SFO. These concentrations increased (P less than 0.05) about twofold after WD. The content of VP, ng/g wet weight, in HC-F was higher (P less than 0.05) than the SFO area and also increased (P less than 0.05) after WD. VP was detected in other fiber tracts, anterior commissure (AC) and fornix (F), but was unchanged by WD. Changes in hormone observed in the SFO and HC-F regions were therefore not part of a generalized increase of VP in the brain, nor can they be ascribed to elevated plasma levels. Thus, VP changes in the SFO region may be functionally significant and related to an SFO endocrine role in hydration. VP in fiber tracts (F, AC) unassociated with the hypothalamo-hypophysial system and unchanged after WD may suggest an unidentified role of this hormone in the central nervous system.

Topics: Animals; Dehydration; Hippocampus; Male; Neural Pathways; Rats; Vasopressins

The neural lobe of the golden hamster contains one major and two minor proteins. The major protein was identified as a neurophysin in view of its electrophoretic properties, its high cysteine content and its depletion from the neural lobe upon saline imbibition. The depletion of neurophysin and vasopressin from the neural lobe and the alterations of several indices of dehydration in the blood of the hamster were less than those found in the rat upon saline imbibition, suggesting that the hamster has a greater ability to adapt to conditions in which water is scarce.

Topics: Animals; Cricetinae; Dehydration; Electrophoresis, Polyacrylamide Gel; Mesocricetus; Neurophysins; Pituitary Gland, Posterior; Rats; Sodium Chloride; Vasopressins

In non-hydrated goats prolonged (3 h, 0.02 ml/min) intracerebroventricular (IVT) infusion of 0.35 M glycerol depressed the plasma vasopressin level during the entire infusion period which resulted in a conspicuous water diuresis outlasting the infusion by about 20 min. Since no compensatory drinking occurred during this sustained water diuresis it gradually induced pronounced dehydration (loss of greater than 1 liter of total body water causing 5% increase in plasma [Na+] and osmolality). The same degree of dehydration was in other experiments induced by water deprivation. It then caused a 5-fold increase in plasma vasopressin level. Corresponding IVT infusions of 0.35 M d-glucose depressed plasma vasopressin level only during the first half of the 3 h infusion period. Consequently, the resulting water diuresis was transient and subsided before the glucose infusion was finished. Plasma renin activity increased during the IVT glycerol infusion and during water deprivation, but was largely unaffected by IVT glucose. Both IVT glycerol and glucose decreased renal sodium excretion. The possibility is discussed that the pronounced ability of IVT glycerol to depress the vasopressin release and thirst is not only due to dilution induced reduction of CSF [Na+], but also to an influence of glycerol on choroidal and/or transependymal Na+-transporting mechanisms.

Topics: Animals; Blood; Dehydration; Diuresis; Female; Glucose; Glycerol; Goats; Hypernatremia; Injections, Intraventricular; Osmolar Concentration; Potassium; Sodium; Vasopressins; Water Deprivation

Two patients with hypodipsia and hypernatremia are described. The first patient, whose hypodipsia was of unknown cause, developed hypernatremia unless large volumes of fluid were urged upon him; upon treatment with chlorpropamide normal serum sodium levels were achieved with spontaneous fluid intake. The second patient had hypodipsia and diabetes insipidus resulting from a craniopharyngioma. Treatment with vasopressin and a prescribed daily water intake resulted in frequent hyper- and hyponatremia, but treatment with chlorpropramide yielded serum sodium values which were more often normal and less variable. In neither patient could the improved water regulation be attributed to an effect of chlorpropamide on renal water excretion. Possible mechanisms for the effect of chlorpropamide on thirst are discussed.

Topics: Adult; Chlorpropamide; Dehydration; Diabetes Insipidus; Humans; Hypernatremia; Male; Sodium; Thirst; Vasopressins

Antisera, with cross reactive antibodies removed by affinity chromatography, were used in the immunoperoxidase-bridge technique to study the distribution of oxytocin and vasopressin together with neurophysin in the hypothalamo-neurohypophysial system of the rat. The hormones were demonstrated in different areas of the supraoptic nucleus (SON) and paraventricular nucleus (PVN), in neurosecretory fibres of the hypothalamo-neurohypophysial tract, median eminence, and in nerve terminals of the neurohypophysis. Intact normal and rats with hereditary hypothalamic diabetes insipidus (Brattleboro strain), and rats dehydrated by the administration of oral hypertonic saline were studied. In dehydrated rats the hormone concentration in the neurons, and the number of neurons containing hormone varied according to the time of dehydration stress. The observations support the hypotheses that: 1) oxytocin and oxytocin-neurophysin, and vasopressin and vasopressin-neurophysin are synthesised in different neurons and are transported along different axons; 2) the SON and PVN are functionally indistinguishable in that neurons containing oxytocin or vasopressin are present in both nuclei; and 3) the two types of neurons respond to osmotic stimulation in a way that is qualitatively the same but quantitatively different.

Topics: Animals; Dehydration; Diabetes Insipidus; Female; Fluorescent Antibody Technique; Hypothalamo-Hypophyseal System; Immunoenzyme Techniques; Median Eminence; Neurons; Neurophysins; Oxytocin; Paraventricular Hypothalamic Nucleus; Pituitary Gland, Posterior; Rats; Rats, Inbred Strains; Supraoptic Nucleus; Vasopressins

The development of a sensitive radioimmunoassay for plasma arginine vasopressin (pAVP) is described. Using this assay, the levels of vasopressin were determined in the plasma of nondehydrated and dehydrated rats after exposure to ether or acceleration stress. Plasma AVP was also determined in rats following nicotine administration. Nondehydrated rats showed no significant changes in pAVP 1, 2, 5, or 15 min after exposure to ether for 1 min. Dehydrated rats, on the other hand, had significantly reduced pAVP after exposure to ether. One group (180-220 g) showed a decline in pAVP of 27% at 2 min (P less than 0.05) and and 47% at 5 min (P less than 0.001) after stress. In a group of larger animals (350-400 g), pAVP levels were reduced by 55% at 1 min (P less than 0.05) and 72% at 2 min (P less than 0.01) after ether stress. A third group (250-300 g) also had significantly reduced pAVP values of 57% (P less than 0.01) 5 min after ether stress but not at 15 min. Nondehydrated rats which were centriguated at -4.1 Gx for 5, 15 or 120 min showed no significant alterations in pAVP. No decrease in pAVP was observed in dehydrated rats centrifugated for 5 min; after 120 min of centrifugation, mean pAVP was reduced by 40% (P less than 0.02) when compared to be noncentrifugated controls. In contrast to either ether or acceleration stress, nicotine provoked a marked rise (P less than 0.005) in pAVP 10 min after injection. From these results it was concluded that ether or acceleration stress does not evoke an increase in the pAVP levels of rats, and furthermore, in dehydrated rats, these stressors will produce a significant decline in pAVP.

Topics: Animals; Arginine Vasopressin; Dehydration; Ether; Female; Male; Nicotine; Radioimmunoassay; Rats; Rotation; Stress, Physiological; Vasopressins

The brain has evolved a number of mechanisms to maintain body fluid balance. They include the sensation of thirst, which stimulates water intake, the secretion of vasopressin, which helps prevent water loss, and the secretion of aldosterone, which helps prevent sodium depletion. In the research described here, all three mechanisms are shown to be mediated by the actions of angiotensin on the brain.

Topics: Aldosterone; Angiotensin II; Animals; Brain; Dehydration; Dogs; Drinking; Extracellular Space; Humans; Intracellular Fluid; Osmolar Concentration; Renin; Sodium; Thirst; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Arginine Vasopressin; Body Weight; Dehydration; Glomerular Filtration Rate; Inulin; Kinetics; Osmolar Concentration; Pituitary Gland, Posterior; Salamandridae; Skin; Skin Physiological Phenomena; Sodium Chloride; Sucrose; Urinary Bladder; Urodela; Vasopressins; Water-Electrolyte Balance

Three cases of compulsive polydipsia previously diagnosed as diabetes insipidus are presented. Abnormally dilated bladder and pyelocalyceal systems were accompanying features, as previously described for diabetes insipidus, particularly of renal orign. Results of the hypertonic saline (Hickey-Hare) test were positive in only one case. Results of restriction of liquids followed by intravenous injection of vasopressin (Miller test) favoured a diagnosis of complete diabetes insipidus. These two tests cannot, therefore, exclude compulsive polydipsia. The features suggesting a diagnosis of compulsive water drinking are low plasma osmolality, a decrease in 24-hour urine output following water restriction, and abnormal behaviour. The diagnosis is confirmed by an 18-hour dehydration test done after gradual fluid restriction, which favours partial restoration of the papillary osmotic gradient.

Topics: Adolescent; Compulsive Behavior; Dehydration; Diabetes Insipidus; Diagnosis, Differential; Drinking; Female; Humans; Hydronephrosis; Hypertonic Solutions; Infusions, Parenteral; Middle Aged; Osmolar Concentration; Urinary Bladder Diseases; Vasopressins

Topics: Adrenalectomy; Animals; Dehydration; Dexamethasone; Diabetes Insipidus; Homozygote; Hypothalamo-Hypophyseal System; Median Eminence; Neurophysins; Rats; Vasopressins

The plasma arginine vasopressin (pAVP) response to osmotic stimulation was studied in dogs and sheep by sampling at frequent intervals during steady-state dehydration and during water diuresis. Frequent sampling also was conducted after continuous infusion or bolus injection of 5 or 20 g/100 ml NaCl. A pulsatile pattern of pAVP was observed after such infusions or injections and in some animals after water deprivation. This pattern was not seen after water loading or in mildly dehydrated animals. The short term changes in pAVP during continuous infusion of 5 g/100 ml NaCl could not be correlated with variations in plasma tonicity. Rather, they appeared to reflect discontinuous hypothalamic posterior pituitary release of AVP. Thirst was evoked by a lower dose of 5 g/100 ml NaCl than was required for consistent stimulation of pAVP release, and the thirst response frequently was observed prior to the peak AVP response after bolus injection of 5 and 20 g/100 ml NaCl.

Topics: Animals; Arginine Vasopressin; Dehydration; Dogs; Osmolar Concentration; Saline Solution, Hypertonic; Sheep; Sodium; Sodium Chloride; Vasopressins; Water

The integrated plasma arginine vasopressin concentration (IpAVP) was determined by pooling the results of single samples collected every 3 min for 0.5 h in dehydrated, randomly hydrated, and water-loaded sheep. A linear relationship was observed between the log of the integrated AVP concentration and plasma osmolality. This relationship was tested by the bolus injection of 20 g/100 ml NaCl to both water-loaded and randomly hydrated sheep. The rise in the log of IpAVP divided by the rise in plasma osmolality was similar in both groups (P greater than 0.5) and was superimposable upon the regression line derived from steady-state observations. The data would suggest that AVP is released as an exponential function of plasma osmolality rather than as a threshold phenomenon.

Topics: Animals; Arginine Vasopressin; Dehydration; Female; Osmolar Concentration; Saline Solution, Hypertonic; Sheep; Sodium Chloride; Vasopressins; Water

Plasma arginine vasopressin concentrations were measured in five healthy volunteers during postural change under conditions of dehydration and normal hydration. A rise in plasma arginine vasopressin was observed only after dehydration and standing for 40 min. Five further volunteers who developed presyncopal symptoms during orthostasis had exceedingly high plasma arginine vasopressin levels. Changes in plasma arginine vasopressin concentration occurred with no signficant alterations in plasma osmolality.

Topics: Arginine Vasopressin; Dehydration; Female; Humans; Male; Posture; Syncope; Time Factors; Vasopressins

A radioimmunoassay for AVP capable of measuring human plasma AVP is described. Iodination was performed by the chloramine T method and purified by chromatography on Sephadex G-25. Specific activity of 125I-AVP was 1710 +/- 155 Ci/mmol. Antiserum of high affinity (Keq = 2.7 X 10(11) 1/mol) has been raised in rabbits, which shows slight cross-reactivity with LVP and negligible reactivity with oxytocin. The aqueous assay is capable of detecting 0.4 fmol of AVP/tube and it is highly reproducible. A F lorisil extraction technique is described in detail and gives recovery of 70% of synthetic AVP added to plasma over a wide physiological range. The lowest detectable concentration of plasma AVP is 0.3 pmol/l. The method has been validated by studying changes in plasma AVP concentration following overnight dehydration (plasma AVP =3.46 +/- 1.89 (SD) pmol/l), and water loading (plasma AVP = 1.54 +/- 0.59 pmol/l), P less than 0.005, in normal subjects. A highly significant positive correlation has been found between plasma AVP and plasma osmolality (r =+0.75). Plasma AVP concentration has also been determined in patients with DI and the syndrome of inappropriate ADH secretion. No effect was found on the level of plasma AVP in normally hydrated volunteers undergoing postural change but levels rose following strenuous exercise from basal concentrations of 1.57 +/- 0.59 pmol/l to 4.77 +/- 3.43 pmol/l, P less than 0.01.

Topics: Arginine Vasopressin; Dehydration; Diabetes Insipidus; Humans; Immune Sera; Osmolar Concentration; Physical Exertion; Posture; Radioimmunoassay; Vasopressins

Two female reindeer were hydrated by administration of (10% of b.wt.) water into the rumen. The diuretic response was very fast and strong but the urea and electrolyte excretion were little affected. Dehydration was carried out by not giving the reindeer water for 48 h. This water deprivation caused a loss of up to 20% of their body weight. The urine osmolality did not exceed 840 mosm/kg H2O, although the plasma osmolality rose from 300 to 346 and 368 mosm/kg H2O respectively. The plasma and urine urea concentrations were elevated during dehydration, while the urine urea excretion did not increase. Urine sodium concentration did not increase. When the urine flow rate, after two days of water deprivation, decreased to half of the original, the urine Na+ concentrations, instead of increasing, went down to half of the original. So did the potassium excretion. When ADH was injected intravenously into hydrated animals a dose of 30 mU of ADH was needed to induce antidiuresis or increased excretion of potassium. The resistance to ADH and the low relative thickness of the medulla confirm the limited capacity of reindeer kidney to concentrate urine or to excrete a solute load. On the other hand, reindeer is able rapidly to excrete surplus water without affecting the electrolyte or nitrogen balance.

Topics: Animals; Dehydration; Diuresis; Electrolytes; Kidney; Osmolar Concentration; Reindeer; Vasopressins; Water-Electrolyte Balance

Topics: Dehydration; Diagnosis, Differential; Humans; Hyponatremia; Infant, Newborn; Infant, Premature, Diseases; Syndrome; Vasopressins

Vasopressin and oxytocin were measured by radioimmunoassay in rat posterior pituitary and microdissected hypothalamic areas after 3 and 10 days of oral 2 percent sodium chloride in place of drinking water. There was a significant decrease in concentration of both hormones in posterior pituitary and in specific areas of the hypothalamus. Supraoptic, paraventricular, and arcuate hypothalamic nuclei and the retrochiasmatic area had decreased concentration of one or both hormones following hypertonic saline, while hormone concentration in the suprachiasmatic nucleus and median eminence was unaffected.

Topics: Administration, Oral; Animals; Dehydration; Hypothalamus; Male; Oxytocin; Pituitary Gland, Posterior; Rats; Saline Solution, Hypertonic; Sodium Chloride; Time Factors; Vasopressins

Unanesthetized dogs were infused with heterologous (hog) renin at 0.33 Goldblatt U/kg per h for 2 h, once normally hydrated and once after 48 h of dehydration. Dehydration increased the average plasma osmolality from 306 to 322 mosmol/kg, the plasma renin activity (PRA) from 0.5 to 1.4 ng/ml per h, and the plasma antidiuretic hormone (ADH) concentration from 1.7 to 3.7 muU/ml, although the latter was not statistically significant. Renin infusion resulted in approximately the same average PRA, about 10 ng/ml per h, in both states of hydration. Mean arterial blood pressure increased during renin infusion in both states of hydration, although the increase was greater when the dogs were normally hydrated. There was no apparent effect of renin infusion on plasma ADH concentration when the dogs were normally hydrated, but in the dehydrated state renin infusion was accompanied by an increase from 3.7 to 6.3 muU/ml in plasma ADH concentrations after 80 min of infusion. There were no apparent changes in plasma osmolality or sodium or potassium concentrations due to the renin infusions; however, plasma osmolality and potassium concentration decreased during the course of the experiment. The results suggest a possible role for the renin-angiotensin system of renin released by the kidney in the control of ADH during dehydration. The metabolic clearance rate of the hog renin was 37 ml/min-kg.

Topics: Animals; Blood Pressure; Dehydration; Dogs; Female; Infusions, Parenteral; Male; Osmolar Concentration; Renin; Vasopressins

Topics: Chlorothiazide; Dehydration; Diabetes Insipidus; Fever of Unknown Origin; Humans; Hypernatremia; Infant, Newborn; Infant, Newborn, Diseases; Male; Renal Tubular Transport, Inborn Errors; Specific Gravity; Vasopressins

1. Rabbit antisera against arginine-vasopressin (AVP) were evaluated for sensitivity and specificity in a radioimmunoassay based on the extraction of AVP from plasma and urine on to Florisil. 2. Comparison of the immunoreactivity of AVP with analogues showed that one antiserum (R2) reacted principally with the hexapeptide ring and another (R4) bound to the tripeptide tail and was reactive with some reduction and hydrolytic products of the native peptide. 3. The minimum amount of AVP measurable in the radioimmunoassay was 1 pg. The extraction of AVP from plasma and urine gave a recovery of 93 per cent (sd 5 per cent). A plasma sample repeatedly assayed with R2 gave a value of 1.4 ng/1 (sd 0.2, n=12). 4. The antiserum specific for the hexapeptide ring (R2) showed that in normal subjects AVP concentration ranged from 3.2 +/- 2.52 ng/1 after dehydration to 0.16 +/- 0.1 ng/1 after water loading.

Topics: Animals; Antibody Formation; Arginine Vasopressin; Dehydration; Humans; Immune Sera; Rabbits; Radioimmunoassay; Vasopressins

1. The rate of renal excretion of arginine-vasopressin was determined during unrestricted fluid intake for 24 h and in response to fluid deprivation for 18 h in nine young men with very mild essential hypertension and compared with that in sixteen normotensive men of similar age. 2. Despite an equivalent osmolar stimulus, excretion of arginine-vasopressin was significantly greater in the reference group than in the reference group. This difference increased progressively with increasing dehydration. 3. We suggest that these findings are mainly due to an increased rate of secretion of arginine-vasopressin in response to mild hydropenia in hypertensive patients and that a moderate increase of release of arginine-vasopressin during periods of fluid deprivation may exert vascular effects and thus influence the perpetuation of hypertension.

Topics: Adult; Arginine Vasopressin; Dehydration; Humans; Hypertension; Male; Osmolar Concentration; Vasopressins

In dehydrated rats both neurohypophysial hormones diminished in hypothalamus as well as in the neurohypophysis. Oxytocin disappearef from the hypothalamus and neurohypophysis at a more rapid rate than vasopressin did. The minimal content of vasopressin and oxytocin in the hypothalamus was observed during 3rd--4th day, but even in extreme dehydration it was found to be relatively high: 65 per cent of vasopressin and 27 per cent of oxytocin as compared with intact animals. At that time the neurohypophysial vasopressin and oxytocin content were almost fully exhausted. In dehydrated and additionally reserpinized animals (10 mg/kg intraperitoneally, then each 48 hr 5 mg/kg of initial body weight) the vasopressin and and oxytocin hypothalamus and neurohypophysis changed in a similar manner. In some experimental groups the decrease of neurohormones in both sites was more marked under reserpine treatment. The drug seems therefore rather to potentiate the effects of physiological stimulation of osmodetectors. So the existence of monoaminergic stimulatory synapses, directly involved in the neural pathway between the osmodetector and the neurosecretory cell, appears to be hardly probable.

Topics: Animals; Dehydration; Hypothalamo-Hypophyseal System; Male; Oxytocin; Rats; Reserpine; Vasopressins

A sensitive and specific radioimmunoassay for arginine vasopressin (AVP) was developed utilizing the antisera against lysine vasopressin (LVP) in combination with a labeled AVP. The assay employs an acetone extraction procedure and detects as little as 0.8 pg. per milliliter of AVP in human plasma. In normal subjects the mean (+/- S.D.) plasma concentration of AVP was 4.9 +/- 1.2 pg. per mililiter after fluid deprivation and 1.2 +/- 0.4 pg. per milliliter after water loading. Plasma AVP levels correlated significantly with plasma osmolalities. In four patients with diabetes insipidus, plasma AVP concentrations ranged from less than 0.8 to 1.2 pg. per milliliter, whereas six patients with the syndrome of inappropriate ADH secretion showed plasma levels of AVP which correspond to those of the dehydrated state in normal subjects or greater, although plasma osmolalities were low in all cases. It was concluded that the present radioimmunoassay method for AVP provides a useful way of assessing neurohypophyseal function in man.

Topics: Arginine Vasopressin; Dehydration; Diabetes Insipidus; Humans; Lypressin; Osmolar Concentration; Radioimmunoassay; Vasopressins

To investigate the interaction between antidiuretic hormone (ADH) and renin-angiotensin system, plasma ADH and plasma renin activity (PRA) were determined in normal subjects (n = 10) under various hydrated states. Four experimental conditions, i.e., water loading, infusion of hypertonic saline, acute dehydration induced by furosemide and postural changes, were chosen. 1. Upright posture decreased plasma volume by 9.5 +/- 0.9% without significant changes in plasma osmolality. PRA increased from 5.2 +/- 0.7 to 8.3 +/- 0.8 ng/ml. However, plasma ADH did not change significantly (1.9 +/- 0.3 to 1.8 +/- 0.2 muU/ml). 2. When furosemide was administered intravenously under this condition, both plasma ADH and PRA increased to 3.1 +/- 0.5 muU/ml and 15.5 +/- 1.6 ng/ml with 11.2 +/- 1.1% decrease in plasma volume. Plasma osmolality did not change significantly. 3.Water load resulted in a decrease in plasma osmolality from 282.6 +/- 0.9 to 278.6 +/- 1.2 mOsm/kg without significant change in plasma volume. Significant decrease in plasma ADH level from 2.6 "/- 0.4 to 0.6 "/- 0.1 muU/ml was found, but PRA (7.8 +/- 1.1 ng/ml) did not change (6.3 +/- 1.0 ng/ml). 4. Hypertonic saline infusion brought about an increase in plasma osmolality to 290.1 +/- 0.8 mOsm/kg with simultaneous increase in plasma volume by 6.7 +/- 1.3%. Plasma ADH level also increased to 2.4 +/- 0.3 muU/ml, while PRA decreased to 4.2 +/- 0.3 mg/nl. Accordingly, significant correlation between changes in PRA and plasma ADH level, was not observed. We suggest that plasma osmolality is the dominant variable in regulating plasma ADH level, but in the presence of a sufficient degree of hypovolemia, the osmotic domination was overcome. On the other hand, PRA was strongly influenced by changes in effective blood volume other than changes in plasma osmolality.

Topics: Blood; Dehydration; Drinking; Furosemide; Humans; Osmolar Concentration; Posture; Renin; Saline Solution, Hypertonic; Vasopressins

The effect of blood volume on the osmotic control of the antidiuretic hormone, arginine vasopressin (AVP), has been studied in 18 healthy young adults. Changes in blood osmolality and/or volume were produced by each of 3 procedures--fluid deprivation, orthostasis, and hypertonic saline infusion--and the resultant changes in plasma AVP were measured by radioimmunoassay and expressed as a function of the simultaneous level of plasma osmolality. When the subjects were hydropenic and recumbent, a highly significant correlation between plasma AVP and osmolality was observed that was described by the regression equation y = 0.35 (x -281.0) where y represents the plasma AVP concentration in pg/ml and x the plasma osmolality in mosmol/kg. When these same hydropenic subjects were studied in the upright position, a maneuver that reduces intrathoracic blood volume, plasma AVP and osmolality still showed a significant correlation, but the regression equation describing this relation, y = 0.31 (x -277.8), occupied a position significantly to the left of that found during recumbency. Conversely, when the same subjects were studied during infusion of hypertonic saline, a procedure that increases blood volume, plasma AVP and osmolality again correlated significantly but the regression equation describing this relation, y = 0.32 (x -282), now occupied a position significantly to the right of that obtained during recumbent and hydropenic conditions. These results indicate that moderate increases or decreases in blood volume do influence the osmoregulation of AVP in man, but the effects are relatively small and limited to adjustments in the set of the receptor toward higher or lower levels of osmolality.

Topics: Adult; Arginine Vasopressin; Blood; Blood Volume; Dehydration; Female; Hematocrit; Humans; Male; Osmolar Concentration; Posture; Saline Solution, Hypertonic; Vasopressins

The ultrastructural features of paraventricular (PVN) and supraoptic (SON) neurons and of their axons were studied in lactating and dehydrated rats. Under both conditions of stimulation, the PVN and SON neurons and their axons enlarge. The protein synthesizing apparatus of the neurons becomes activated, but the number of neurosecretory granules (NSG) is decreased. No differences are seen between the PVN and SON neurons during lactation or dehydration. The similarity and simultaneity of the response of the PVN and SON neurons to these two different stimuli is discussed in the light of the theory of nuclear and neuronal specialization for the production of only one hormone. After prolonged lactation of over 2 1/2 weeks' duration, neurons with extreme vacuolation of the rough endoplasmic reticulum (RER) appear in the PVN and SON; the vacuolated neurons appear earlier and predominantly in the PVN involving a maximum of 10-15% of all PVN neurons. Vacuolated neurons were never seen in either nucleus during dehydration of up to 6 days' duration. The vacuolation is suggested to represent an exhaustion phenomenon due to an intense, long-lasting stimulus for oxytocin synthesis. The predominant location of the vacuolated neurons in the PVN supports the theory that oxytocin is produced predominantly in the PVN. The decrease in the number of NSGs during these states of enhanced hormone secretion is considered to corroborate the proposed existence of an extragranular fast axoplasmic transport mechanism in PVN and SON neurons. The possible existence of a reuptake mechanism into NSGs, similar to that in the vesicles of monoaminergic nerve endings is discussed.

Topics: Animals; Axonal Transport; Axons; Cytoplasmic Granules; Dehydration; Endoplasmic Reticulum; Female; Golgi Apparatus; Hypothalamo-Hypophyseal System; Hypothalamus; Lactation; Male; Neurons; Neurophysins; Oxytocin; Paraventricular Hypothalamic Nucleus; Pregnancy; Rats; Supraoptic Nucleus; Vacuoles; Vasopressins

Lithium (Li+) chloride, 2 to 3 mEq. per kilogram of body weight, was administered intraperitoneally to normal Wistar rats daily for 4 to 66 days. This resulted in a marked reduction in urine osmolality (Uosm.) and increase in the excretion of water, Na+, K+, uric acid, and phosphate. The excretion of uric acid and potassium was a direct function of UNaV. The magnitude of depression in urine osmolality was significantly related to the rate of excretion of lithium in the urine, suggesting that the change in water reabsorption is dependent on the presence of the ion in the luminal side of the tubule. During 2 per cent saline diuresis, Li+-treated rats achieved less fractional free water reabsorption (TcH2O/GFR times 100) at any level of fractional osmolar clearance (Cosm./GFR times 100) than normal rats. On the other hand, during 0.225 per cent saline diuresis, fractional free water clearance (CH2O/GFR times 100) was normal over a wide range of fractional urine flow (V/GFR times 100), indicating intact function of the ascending limb of the loop of Henle. The intravenous infusion of vasopressin (VP) or dibutyryl cyclic-adenosine monophosphate (dcAMP) to Li+-treated rats resulted in a modest rise in Uosm. and a reduction in V/GFR times 100 and CH2O/GFR times 100. Although the response to VP appeared earlier than that to dibutyryl cyclic-AMP, the magnitude of the changes in Uosm., V/GFR times 100, and CH2O/GFR times 100 was eventually the same with both substances. Comparison between normal and Li+-treated rats revealed that the response to both VP and dibutyryl cyclic-AMP was blunted, albeit to a greater extent in the former. Inhibition by Li+ of adenylate cyclase will only partially explain the present data. Impairment in the release of endogenous VP or a block distal to the formation of cyclic-AMP must have played a role. In view of a normal diluting capacity and the increase in the excretion of phosphate and uric acid, it is suggested that Li+, when administered chronically in the present doses, inhibits proximal tubular reabsorption.

Topics: Animals; Body Weight; Bucladesine; Dehydration; Female; Kidney; Kidney Concentrating Ability; Kidney Tubules, Distal; Kidney Tubules, Proximal; Lithium; Male; Phosphates; Potassium; Rats; Sodium; Uric Acid; Vasopressins; Water-Electrolyte Balance

A radioimmunoassay has been developed for plasma arginine-vasopressin in man and dog. The mean recovery of added arginine-vasopressin (AVP) was 60 +/-6.9 (S.D.)% and the lower threshold of detection 2.0 pmol/1. A close correlation was found between concurrent radioimmunoassay and bioassay values. The mean concentration found in peripheral venous blood in healthy men after overnight fasting was 5.3 pmol/1 (range 4.6-6.2 pmol/1.) In man, significant increases in plasma AVP occurred after dehydration (5-9-9-5 pmol/1) and significant decreases after oral water-loading (5.9-9.5 pmol/1). During i.v. infusion of graded doses of synthetic AVP in normal men, plasma levels were closely correlated with infusion rate. On stopping the infusion, plasma vasopressin fell exponentially with a half-life of between 7 and 8 min. In man, plasma AVP was unaffected by tilting head-up for 2 h, or by a non-hypotensive bleeding of 500 ml in 10 min. In the dog, haemorrhage of 5 ml/kg and over caused proportionate increases in AVP in the circulation. In normal men, plasma vasopressin was significantly correlated with concurrent urinary osmolality. Five patients with oat-cell bronchial carcinoma and hyponatraemia showed a marked increase of plasma vasopressin. Five patients with diabetes insipidus had significantly reduced, but detectable, levels of plasma AVP. The plasma concentration in these patients did not increase after water restriction.

Topics: Adult; Animals; Arginine Vasopressin; Biological Assay; Blood Volume; Bronchial Neoplasms; Carcinoma, Small Cell; Dehydration; Diabetes Insipidus; Dogs; Half-Life; Hemorrhage; Humans; Male; Osmolar Concentration; Posture; Radioimmunoassay; Urine; Vasopressins; Water; Water Deprivation

Topics: Adult; Age Factors; Coma; Dehydration; Female; Humans; Infant, Newborn; Kidney; Male; Methods; Middle Aged; Neurophysins; Nicotine; Pituitary Gland, Posterior; Pregnancy; Radioimmunoassay; Smoking; Sodium Chloride; Twins; Vasopressins

The renal tubular responsiveness to antidiuretic hormone was assessed in seven obese patients during starvation and feeding by an overnight dehydration test followed by exogenous vasopressin. All seven subjects showed a mean reduction of one-third in their maximum urinary osmolality on day 4 of starvation. Thes- data show that the renal tubule is partially insensitive to antidiuretic hormone at a time when it is also insensitive to mineralocorticoids.?Author

Topics: Adult; Body Weight; Dehydration; Diet; Fasting; Humans; Kidney Tubules; Middle Aged; Mineralocorticoids; Nutritional Physiological Phenomena; Obesity; Osmolar Concentration; Time Factors; Urination; Urine; Vasopressins

Since previous studies from this laboratory have demonstrated that the redistribution of blood volume and concomitant relative central hypervolemia induced by water immersion to the neck causes a profound natriuresis and a suppression of the renin-aldosterone system, it was of interest to assess whether the diuresis induced by immersion was mediated by an analogous inhibition of ADH. The effects of water immersion on renal water handling and urinary ADH excretion were assessed in 10 normal male subjects studied following 14 h of overnight dehydration on two occasions, control and immersion. The conditions of seated posture and time of day were identical. During control ADH persisted at or above prestudy values. Immersion resulted in a progressive decrease in ADH excretion from 80.1 plus or minus 7 (SEM) to 37.3 plus or minus 6.3 muU/min (P smaller than 0.025). Cessation of immersion was associated with a marked increase in ADH from 37.3 +/- 6.3 muU/min to 176.6 +/- 72.6 muU/min during the recovery hour (P smaller than 0.05). Concomitant with these changes urine osmolality decreased significantly beginning as early as the initial hour of immersion from 1044 +/- 36 to 542 +/- 66 mosmol/kg H2O during the final hour of immersion (P smaller than 0.001). Recovery was associated with a significant mean increase in Uosm of 190 +/- 40 mosmol/kg H2O over the final hour of immersion (P smaller than 0.001). The suppression of ADH occurred without concomitant changes in plasma tonicity. These studies are consistent with the suggestion that in hydrated subjects undergoing immersion suppression of ADH release contributes to the enhanced free water clearance, which has been previously documented.

Topics: Adult; Blood Volume; Body Weight; Creatinine; Dehydration; Diuresis; Humans; Immersion; Male; Osmolar Concentration; Potassium; Sodium; Time Factors; Urine; Vasopressins

Thirst stimulation of the supraoptic nucleus (SON) and paraventricular nucleus (PVN) was induced in rats by withholding all fluids during three days. 35S-cysteine was then intraperitoneally administered and the rats were killed at predetermined times and examined by autoradiography, applying the authors' previously described method. This experimental series totalling 51 animals was compared with a control series of 70 rats, similarly treated, who had had free access to water. The kinetic phenomena in SON and PVN were analysed in terms of the two-compartment model previously used, which gives an estimate of the neurosecretory material (NSM) secretion parameters and of those of the lumped structural cell protein turnover in the nuclei. The kinetics of the precursor amino acids after administration of labelled cysteine were also assessed. Determinations of the label uptake at two specific times in the experiment, in the infundibular nucleus, ventromedial nucleus and optic nerve tissue in both series served as a check on the specifity of the structural protein turnover changes observed. Compared with the controls, the turnover rate of the slow compartment was more than tripled in the dehydrated rats, while that of the fast compartment had gone down to about one-third; both effects very nearly equal in SON and PVN. These results are compatible with the concept according to which thirst stimulates the SON and PVN equally. A distinct, and strikingly equal, hump was observed (2 hours after label administration) in all specific activity curves, also in the precursor serum concentration, and it is probably due to recycling of 35s from cysteine to methionine. This and other circumstances render the phenomena rather too complex for a straight-forward evaluation by the two-compartment model. Even so, the observations are believed to furnish good evidence of the biological verity of this model as well as the thirst-induced changes elicited.

Topics: Animals; Cysteine; Dehydration; Hypothalamo-Hypophyseal System; Kinetics; Male; Methionine; Models, Biological; Nerve Tissue Proteins; Paraventricular Hypothalamic Nucleus; Rats; Supraoptic Nucleus; Vasopressins

Studies were performed to determine the mechanism by which the antihypertensive agent clonidine increases urine flow (V). In 11 anesthetized, hydropenic dogs, i.v. administration of clonidine (30 mug/kg) increased arterial pressure from 128 +/- 4 to 142 +/- 3 mm Hg and slowed heart rate from 138 +/- 7 to 95 +/- 7 beats/min within 30 min of injection; blood pressure then fell to 121 +/- 5 mm Hg 30 to 60 min after injection, and 112 +/- 5 mm Hg in the next 30-min period. V increased from 0.36 +/- 0.09 to 0.93 +/- 0.13 Uosm ml/min and urine osmolality (Uopsm) decreased from 1378 +/- 140 to 488 +/- 82 mOsm/kg of H2O 30 to 60 min following injection (P less than 0.001). These changes were accompanied by a decrease in TcH20. This increased V was not associated with increased glomerular filtration rate (GFR) or solute excretion, and occurred in acutely denervated kidneys and kidneys protected from the initial increase in arterial pressure by constriction of a suprarenal aortic clamp. By contrast, V TcH2O and UOsm were not altered by clonidine administration in seven acutely hypophysectomized dogs receiving a constant infusion of antidiuretic hormone (ADH) (80 muU/kg/min), despite similar hemodynamic changes produced by the drug. The results suggest that clonidine increases V through inhibition of ADH release, possibly via an indirect pathway mediated by the drug's alpha-adrenergic on the circulation.

Topics: Animals; Blood Pressure; Clonidine; Dehydration; Depression, Chemical; Diuresis; Dogs; Glomerular Filtration Rate; Heart Rate; Hemodynamics; Hypophysectomy; Kidney; Male; Osmolar Concentration; Potassium; Regional Blood Flow; Urine; Vasopressins; Water-Electrolyte Balance

A 20-yr-old male was found to have diabetes insipidus is association with panhypopituitarism but without any focal neurological lesion being identified. He was initially treated with steroid supplements, the features of diabetes insipidus being controlled with a thiazide diuretic. Eighteen months later the patient lost thirst sensation and stopped treatment, subsequently being re-admitted with severe dehydration, oliguria and focal neurological signs. Further investigation, including brain biopsy, confirmed the presence of an atypical pinealoma which was considered inoperable. Measurements of plasma antidiuretic hormone (ADH) and angiotensin II (AII) concentrations during the severe dehydration showed very high levels of AII, but inappropriately low plasma ADH levels for the severity of dehydration. We consider that the evidence obtained from this case supports the view that the oliguria with hypertonic urine present during severe dehydration was due to a direct renal action of the very high AII levels, possibly supplemented by the residual ADH secretion.

Topics: Adult; Angiotensin II; Circadian Rhythm; Dehydration; Diabetes Insipidus; Growth Hormone; Humans; Hypopituitarism; Male; Osmolar Concentration; Time Factors; Urine; Vasopressins

The fine structure of the pituitary posterior lobe was observed using normal, dehydrated and Pitressin-treated mice. The normal posterior lobe of the mouse contains numerous neurosecretory granules of about 1,300-2,000 angstrom diameter in the nerve terminals. These granules are often found in contact with neurotubules running longitudinally in the axon. In the 2, 5 and 7 day-dehydrated animals the secretory granules are markedly decreased in number, while small vesicles of about 500 angstrom diameter are conspicuously increased in number in the nerve terminal. It is very difficult to obtain an electron microscopic figure of the exocytosis of the secretory granule. The cluster of small vesicles in the nerve terminal is sometimes surrounded by an electron dense membrane and gradually changed to the cytolysomes. These facts suggest that most of these vesicles are not synaptic vesicles containing acetylcholine but materials derived from the limiting membrane of the released granules and they are gradually disposed of by lysosomes. In Pitressin-treated animals (3 days, 200mU/day), an increase in number of the neurosecretory granules and an appearance of the disposal process of the excess neurosecretory granules are characteristic in the nerve terminal. Some granules are aggregated to become higher in electron density and surrounded by an electron dense membrane. They are positive for acid phosphatase reaction and are degenerated by an autolytic process. In both cases above, the pituicytes showed a marked reaction. The elements of rough endoplasmic reticulum and the Golgi apparatus become well developed and many large lysosomes are seen in the cytoplasm.

Topics: Animals; Dehydration; Male; Mice; Pituitary Gland, Posterior; Vasopressins

Topics: Animals; Dehydration; Hyaluronoglucosaminidase; Kidney; Male; Rats; Vasopressins

A radioimmunoassay method for the measurement of arginine-vasopressin (AVP) in human plasma has been developed which requires 5 ml of plasma and has a lower limit of detection of 1-8 pg/ml plasma. Arginine-vasopressin was found to be stable in whole blood for up to 1 h at room temperature and for at least 4 h at 4 degrees C, while in plasma stored at -20 degrees C no loss was seen over 10 days. Dehydration and rehydration in normal subjects produced appropriate changes in AVP concentration but there was considerable variability in the levels attained by individual subjects and no obvious correlation with plasma osmolality. No consistent increase in plasma AVP concentration was seen on change of posture from the recumbent to the upright position. Vigorous exercise produced a marked rise in plasma AVP concentrations in most subjects which could not be attributed simply to an increase in plasma osmolality. In fusion studies with Pitressin in normal subjects showed a mean half-life of 6-4 min with an overall plasma clearance rate of 8-5 ml/min/kg body weight and a mean volume of distribution of 5-33 l. In patients with a biochemical picture suggestive of inappropriate antidiuretic hormone secretion, markedly raised plasma AVP concentrations were found only in patients with bronchial carcinoma.

Topics: Arginine Vasopressin; Blood Preservation; Bronchial Neoplasms; Dehydration; Furosemide; Growth Hormone; Humans; Hydrocortisone; Hyponatremia; Leukemia; Osmolar Concentration; Physical Exertion; Posture; Radioimmunoassay; Thyrotropin; Urine; Vasopressins

Topics: Animals; Arginine Vasopressin; Circadian Rhythm; Dehydration; Diabetes Insipidus; Heterozygote; Homozygote; Rats; Vasopressins

Topics: Ammonia; Animals; Anura; Dehydration; Mathematics; Osmotic Pressure; Rana pipiens; Seasons; Time Factors; Urea; Vasopressins

Topics: Benzothiadiazines; Body Water; Carcinoma, Bronchogenic; Chlorpropamide; Dehydration; Diuretics; Edema; Humans; Hyponatremia; Sodium; Sodium Chloride Symporter Inhibitors; Vasopressins; Water Intoxication

Topics: Animals; Arginine; Dehydration; Diuresis; Female; Male; Natriuresis; Skin; Sodium; Sodium Chloride; Urinary Bladder; Urodela; Vasopressins; Water; Water-Electrolyte Balance

Topics: Administration, Intranasal; Adolescent; Child; Child, Preschool; Dehydration; Humans; Infant; Infant, Newborn; Injections; Injections, Intravenous; Kidney Concentrating Ability; Methods; Osmolar Concentration; Sodium; Vasopressins; Water Deprivation

Topics: Adrenal Glands; Animals; Body Weight; Dehydration; Diabetes Insipidus; Drinking; Drug Resistance; Eating; Female; Kidney Glomerulus; Kidney Medulla; Kinetics; Male; Mice; Mice, Inbred C3H; Mice, Inbred C57BL; Mice, Inbred Strains; Osmolar Concentration; Sodium Chloride; Vasopressins; Water; Water Deprivation

Topics: Animals; Body Weight; Dehydration; Drinking Behavior; Environment, Controlled; Environmental Exposure; Feeding Behavior; Hypothermia; Hypoxia; Kidney; Kidney Concentrating Ability; Male; Organ Size; Osmolar Concentration; Oxygen Consumption; Rats; Regression Analysis; Time Factors; Urination; Vasopressins; Water

Topics: Animals; Blood Volume; Body Water; Dehydration; Dogs; Sodium Chloride; Sympathetic Nervous System; Thirst; Vagotomy; Vagus Nerve; Vasopressins; Water-Electrolyte Balance

Topics: Amines; Animals; Biological Transport; Carbon Radioisotopes; Dehydration; Disease Models, Animal; Glomerular Filtration Rate; Inulin; Kidney; Kidney Concentrating Ability; Kidney Cortex; Kidney Diseases; Kidney Medulla; Kidney Tubules; Male; Microscopy, Electron; Osmolar Concentration; Photometry; Potassium; Punctures; Quaternary Ammonium Compounds; Rats; Sodium; Thiazoles; Urea; Vasopressins; Water

Topics: Animals; Antibody Specificity; Arginine; Chickens; Chromatography, Paper; Dehydration; Immune Sera; Iodine Radioisotopes; Oxytocin; Pituitary Gland; Rabbits; Radioimmunoassay; Rana catesbeiana; Rats; Time Factors; Vasopressins; Vasotocin

Topics: Animals; Body Temperature Regulation; Dehydration; Diuresis; Dogs; Drinking; Hot Temperature; Hypothalamo-Hypophyseal System; Male; Pituitary Gland; Sodium Chloride; Thirst; Vasopressins

Topics: Animals; Cat Diseases; Cats; Chronic Disease; Dehydration; Diabetes Insipidus; Hydrochlorothiazide; Kidney Diseases; Male; Urine; Vasopressins

Topics: Animals; Body Weight; Dehydration; Female; Gerbillinae; Humidity; Hypothalamo-Hypophyseal System; Kidney; Male; Vasopressins

Topics: Adult; Arrhythmias, Cardiac; Central Nervous System Diseases; Dehydration; Diabetes Insipidus; Electrocardiography; Female; Humans; Hypokalemia; Vasopressins

Topics: Adult; Body Fluids; Body Weight; Creatinine; Dehydration; Glomerular Filtration Rate; Humans; Kidney Concentrating Ability; Male; Osmolar Concentration; Physical Exertion; Potassium; Sodium; Steam Bath; Temperature; Vasopressins

Topics: Adrenocorticotropic Hormone; Aldosterone; Catecholamines; Craniocerebral Trauma; Dehydration; Electrolytes; Glucagon; Glucose; Growth Hormone; Humans; Hydrocortisone; Hypernatremia; Hyponatremia; Metabolic Diseases; Vasopressins; Water Intoxication; Water-Electrolyte Balance

Topics: Animals; Biological Assay; Dehydration; Diabetes Insipidus; Humans; Hypophysectomy; Pituitary Gland; Radioimmunoassay; Rats; Time Factors; Vasopressins; Water Deprivation; Water-Electrolyte Balance

Topics: Animals; Body Weight; Cats; Dehydration; Disease Models, Animal; Hypernatremia; Hypothalamus; Natriuresis; Osmolar Concentration; Potassium; Silver Nitrate; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Chlorides; Creatine; Dehydration; Desoxycorticosterone; Diet, Sodium-Restricted; Natriuresis; Osmolar Concentration; Potassium; Rats; Urea; Vasopressins; Water-Electrolyte Balance

Normal subjects and patients with antidiuretic hormone (ADH) deficiency were studied to determine the mechanism of the antidiuretic action of clofibrate. Before clofibrate treatment, the patients' ability to concentrate urine with a standardized dehydration procedure correlated with the amount of ADH which was excreted. During clofibrate administration all six patients with ADH deficiency developed an antidiuresis which was like that of ADH, since there was no change in sodium, potassium, total solute, or creatinine excretion. There was a correlation between the patients' ability to concentrate urine during dehydration and the subsequent response to clofibrate, and the excretion of ADH during dehydration correlated with the excretion of ADH on clofibrate therapy. Clofibrate-induced antidiuresis in these patients was partially overcome by ethanol and by water loading. Clofibrate interfered with the ability of patients and subjects to excrete a water load and prevented the water load from inhibiting ADH excretion in the normal subjects. These studies suggested that clofibrate was acting through endogenous ADH and this thesis was supported by the failure of clofibrate to produce an antidiuresis when injected into rats with total ADH deficiency (Brattleboro strain) although an antidiuresis was produced in water-loaded normal rats. When the drug was injected into Brattleboro rats with exogenous ADH, clofibrate either did not alter or it inhibited the action of the ADH. The data demonstrate that clofibrate has a significant ADH-like action. This action appears to be mediated through the release of endogenous ADH.

Topics: Adult; Animals; Clofibrate; Creatinine; Dehydration; Diabetes Insipidus; Diuresis; Drinking; Ethanol; Female; Humans; Male; Middle Aged; Osmolar Concentration; Potassium; Rats; Sodium; Urination; Vasopressins

Topics: Adult; Dehydration; Diet Therapy; Diuretics; Ethanol; Humans; Hypernatremia; Male; Muscular Diseases; Natriuresis; Osmolar Concentration; Paralysis; Potassium; Sodium; Vasopressins; Water Intoxication

Topics: Acid-Base Equilibrium; Acidosis; Ammonia; Animals; Dehydration; Dogs; Extracellular Space; Glutamates; Glutaminase; Glutamine; Hydrogen-Ion Concentration; Kidney; Kidney Cortex; Kidney Medulla; Male; Phosphates; Rats; Vasopressins; Water

Twenty cases of familial ADH-responsive diabetes insipidus were identified within five generations, and eight patients were studied by one of two established dehydration protocols. In each case there was partial to total failure of response to the initial administration of ADH which was slowly corrected by continued administration. This initial failure can lead to misinterpretation of the dehydration test unless the medullary solute washout effect is taken into account in chronically polyuric patients.Treatment consisted of thiazides and/or chlorpropamide. All cases responded well.The response to chlorpropamide suggests that the failure of ADH production is not complete in these patients, and that the major defect is a failure of ADH release in response to normal stimuli. Chlorpropamide may act by either facilitating ADH release or by synergistically interacting with available ADH at the tubular level.

Topics: Adolescent; Adult; Chlorpropamide; Dehydration; Diabetes Insipidus; Female; Humans; Hydrochlorothiazide; Male; Osmolar Concentration; Pedigree; Vasopressins; Water Deprivation

Topics: Animals; Cell Nucleolus; Dehydration; Disease Models, Animal; Hypothalamus; Male; Neurosecretory Systems; Rats; Time Factors; Vasopressins; Water Deprivation; Water-Electrolyte Balance

Topics: Aminohippuric Acids; Animals; Chlorides; Dehydration; Dietary Proteins; Glomerular Filtration Rate; Glucose; Hydrolases; Kidney; Kidney Concentrating Ability; Mannitol; Phosphoenolpyruvate Carboxykinase (GTP); Potassium; Regional Blood Flow; Sheep; Sodium; Starvation; Transferases; Urea; Vasopressins

Topics: Aerospace Medicine; Body Fluids; Body Weight; Conjunctiva; Dehydration; Diuresis; Environment; Humans; Humidity; Lip; Male; Mucous Membrane; Nasal Mucosa; Pharynx; Temperature; Time Factors; Vasopressins; Water-Electrolyte Balance

Topics: Aged; Dehydration; Female; Humans; Kidney; Male; Osmolar Concentration; Osmosis; Pituitary Gland, Posterior; Thirst; Vasopressins; Water Deprivation

Topics: Adipose Tissue; Animals; Dehydration; Fatty Acids, Nonesterified; Female; In Vitro Techniques; Lipid Mobilization; Male; Oxytocin; Pituitary Hormones, Posterior; Rats; Vasopressins

Topics: Adrenocorticotropic Hormone; Animals; Dehydration; Depression, Chemical; Female; Hypertonic Solutions; Hypothalamus; Male; Shrews; Sodium Chloride; Vasopressins

Topics: Animals; Dehydration; Ethanol; Female; Hypothalamus; Male; Neurosecretory Systems; Shrews; Vasopressins

Topics: Adolescent; Albumins; Body Water; Chronic Disease; Circadian Rhythm; Dehydration; Diabetes Insipidus; Glucose Tolerance Test; Humans; Hypernatremia; Hypogonadism; Hypothalamus; Intellectual Disability; Kidney Diseases; Male; Obesity; Polyuria; Renin; Sodium; Thirst; Vasopressins

Topics: Animals; Colon; Colonic Diseases, Functional; Dehydration; Fasting; Gastrointestinal Motility; In Vitro Techniques; Lysine; Muscle Tonus; Rats; Vasopressins

Topics: Adolescent; Adult; Aged; Blood; Child; Dehydration; Female; Glomerular Filtration Rate; Humans; Iodine Radioisotopes; Iothalamic Acid; Kidney Concentrating Ability; Kidney Failure, Chronic; Kidney Medulla; Loop of Henle; Male; Middle Aged; Osmolar Concentration; Polycystic Kidney Diseases; Sodium; Sodium Chloride; Urine; Vasopressins; Water

Topics: Administration, Oral; Adult; Animals; Blood; Cattle; Chromatography; Dehydration; Humans; Iodine Isotopes; Osmolar Concentration; Pituitary Gland; Radioimmunoassay; Sleep; Tissue Extracts; Vasopressins; Wakefulness; Water

1. The method of sequential centrifugation has been used to obtain fluid samples from both the renal papilla and inner medulla of the rat.2. Experiments were carried out on Brattleboro rats with hereditary hypothalamic diabetes insipidus (DI; homozygous recessive), and on their (heterozygous) litter-mates with normal quantities of neurohypophysial vasopressin. Initial classification of the animals by measurement of urine volume and osmolality was confirmed by post-mortem bio-assay of the pituitary glands, in thirty-five out of forty-seven animals.3. In rats with DI, urine osmolalities comparable to those of heterozygous rats were obtained after four daily injections of 1 u. Pitressin Tannate in Oil (PTO). Under these conditions, when dehydration was superimposed for 72 hr, urine osmolality did not increase markedly. In heterozygous rats dehydrated for the same period of time, urine osmolality increased by some twofold.4. In rats with DI, the administration of PTO induced a rise of both sodium and urea concentrations in renal fluids and in urine. Dehydration during PTO administration caused a further rise of urea concentrations only. Dehydration per se significantly raised urinary and renal fluid urea concentrations, but sodium concentrations did not rise.5. In heterozygous rats dehydration per se increased both urea and sodium concentrations in renal fluids and urine.6. The evidence is discussed that the action of vasopressin involves factors apart from increasing the permeability of the distal nephron to water and urea.

Topics: Ammonia; Animals; Centrifugation, Density Gradient; Creatinine; Dehydration; Diabetes Insipidus; Kidney; Natriuresis; Osmolar Concentration; Pituitary Gland; Potassium; Rats; Sodium; Urea; Urine; Vasopressins

Topics: Animals; Cold Temperature; Dehydration; Dietary Fats; Drinking Behavior; Feeding Behavior; Kidney; Male; Osmolar Concentration; Rats; Rheology; Thirst; Urine; Vasopressins; Water Deprivation; Water-Electrolyte Balance

Topics: Dehydration; Diabetes Insipidus; Humans; Methods; Thirst; Vasopressins

Topics: Adrenal Glands; Animals; Dehydration; Diuresis; Dogs; Humans; Kidney; Osmolar Concentration; Pituitary Gland; Thirst; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Blood Proteins; Calcium; Cerebral Cortex; Dehydration; Drug Synergism; Electric Stimulation; Electrophoresis; Female; Hypothalamus; Iodine Isotopes; Lactation; Magnesium; Mesencephalon; Molecular Weight; Pituitary Hormones, Posterior; Potassium; Pregnancy; Protein Binding; Radioimmunoassay; Rats; Reticular Formation; Sodium; Stimulation, Chemical; Swine; Vasopressins

Topics: Animals; Antibodies; Cytoplasm; Dehydration; Hypothalamo-Hypophyseal System; Hypothalamus; Immune Sera; Male; Neurophysins; Pituitary Gland, Posterior; Rabbits; Rats; Sheep; Swine; Vasopressins

Topics: Animals; Autoradiography; Cytoplasm; Dehydration; Diuresis; Epithelium; Female; Histocytochemistry; Kidney Tubules; Male; Osmolar Concentration; Rats; Sulfates; Sulfur Isotopes; Vasopressins

Topics: Blood; Dehydration; Dialysis; Ethanol; Humans; Nephrectomy; Osmolar Concentration; Sodium; Urea; Vasopressins; Water

Topics: 17-Hydroxycorticosteroids; 17-Ketosteroids; Adult; Blood Glucose; Calcinosis; Dehydration; Diabetes Insipidus; Follicle Stimulating Hormone; Glucose Tolerance Test; Growth Hormone; Humans; Hypopituitarism; Hypothalamus; Insulin; Iodine Isotopes; Luteinizing Hormone; Male; Radiography; Skull; Tuberculosis, Meningeal; Vasopressins

Topics: Adult; Altitude; Blood Urea Nitrogen; Body Weight; Carbon Dioxide; Dehydration; Diuresis; Furosemide; Heart Rate; Hematocrit; Hemoglobinometry; Humans; Hypoxia; Male; Oxygen; Partial Pressure; Plasma Volume; Time Factors; Vasopressins; Water

Topics: Adipose Tissue; Animals; Catecholamines; Cycloheximide; Dehydration; Epididymis; Fasting; Fatty Acids, Nonesterified; Female; Male; Oxytocin; Phenoxybenzamine; Pituitary Hormones, Posterior; Propranolol; Rats; Uterus; Vasopressins

Topics: Brain Neoplasms; Child; Chlorpropamide; Craniopharyngioma; Cysts; Dehydration; Diabetes Insipidus; Drinking Behavior; Female; Humans; Kidney Concentrating Ability; Male; Obesity; Osmolar Concentration; Sodium; Thirst; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Arginine; Blood Pressure; Chickens; Chlorides; Dehydration; Female; Glomerular Filtration Rate; Kidney; Male; Natriuresis; Osmolar Concentration; Peptides; Pituitary Hormones, Posterior; Potassium; Urea; Vasopressins; Vasotocin; Water-Electrolyte Balance

Topics: Animals; Cysteine; Dehydration; Electrophoresis, Disc; Hydrogen-Ion Concentration; Oxytocin; Pituitary Hormones, Posterior; Rats; Serum Albumin; Sulfur Isotopes; Vasopressins

1. Rat neurohypophysial extracts have been examined by polyacrylamide-gel electrophoresis. 2. Three of the proteins were tentatively identified as neurophysins by their acidic nature and their disappearance after dehydration of the animals. 3. These proteins were radioactive 24h after intracisternal injection of [(35)S]cysteine. 4. Two of the proteins were present in much greater quantities than the third, and these two were present in the gland in the same ratio as the hormones vasopressin and oxytocin. 5. One of these proteins was absent from glands of rats homozygous for diabetes insipidus but present in heterozygous animals. 6. It is suggested that these two proteins are the vasopressin-neurophysin and oxytocin-neurophysin of the rat.

Topics: Animals; Cysteine; Dehydration; Diabetes Insipidus; Electrophoresis, Disc; Heterozygote; Homozygote; Oxytocin; Pituitary Gland, Posterior; Protein Binding; Protein Biosynthesis; Proteins; Rats; Sulfur Isotopes; Swine; Vasopressins

Topics: Adipose Tissue; Animals; Dehydration; Epinephrine; Fatty Acids, Nonesterified; Lysine; Oxytocin; Phenoxybenzamine; Propranolol; Rats; Vasopressins

Topics: Age Factors; Animals; Animals, Newborn; Cattle; Dehydration; Female; Fetus; Hypertonic Solutions; Lactation; Oxytocin; Pregnancy; Protein Binding; Proteins; Radioimmunoassay; Sodium Chloride; Statistics as Topic; Vasopressins

Topics: Blood; Brain Neoplasms; Child; Dehydration; Glioma; Humans; Hyponatremia; Hypothalamus; Osmolar Concentration; Sodium; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Blood Volume; Dehydration; Humans; Hypertonic Solutions; Male; Osmolar Concentration; Plasma Volume; Sodium Chloride; Vasopressins

1. The changes in urinary and renal tissue composition induced by continuous, intravenous infusion of lysine-vasopressin (60 mu-u./min. 100 g body wt. until steady-state conditions prevailed) in normally hydrated, hydropaenic, saline-loaded (0.9%, w/v) and mannitol-loaded (15%, w/v) rats were determined and compared with those induced in water-loaded rats.2. Previous reports that the urinary responses to antidiuretic hormones vary both with hydration status and with concurrent solute excretion rate were confirmed.3. The data show that variations in urinary responses were accompanied by differences in the papillary responses to lysine-vasopressin.4. The results are discussed in terms of the effects of hydration and concurrent solute excretion on factors influencing (a) medullary accumulation of water and solute, (b) osmotic water reabsorption and (c) osmotic equilibration across the collecting duct; and of the effects of lysine-vasopressin on these factors.5. It is concluded that the effects of hydration and solute excretion on the antidiuretic responses to lysine-vasopressin may be interpreted by differences in (a) the medullary composition prevailing at the start and (b) any further changes in medullary composition that can be induced under the experimental circumstances.

Topics: Animals; Dehydration; Kidney; Lysine; Male; Mannitol; Osmolar Concentration; Potassium; Quaternary Ammonium Compounds; Rats; Sodium; Sodium Chloride; Urea; Vasopressins; Water-Electrolyte Balance

Topics: Blood; Dehydration; Homeostasis; Humans; Osmolar Concentration; Osmotic Pressure; Postoperative Complications; Surgical Procedures, Operative; Urine; Vasopressins; Water Intoxication; Water-Electrolyte Balance

Topics: Animals; Dehydration; Diabetes Insipidus; Kidney; Rats; Sodium; Urea; Vasopressins

Topics: Adult; Dehydration; Humans; Hypernatremia; Hypopituitarism; Hypothalamus; Male; Osmolar Concentration; Pinealoma; Thirst; Vasopressins

Topics: Adrenal Glands; Adrenalectomy; Adrenocorticotropic Hormone; Animals; Corticotropin-Releasing Hormone; Dehydration; Diabetes Insipidus; Female; Formaldehyde; Hypertrophy; Hypothalamo-Hypophyseal System; Hypothalamus; Karyometry; Kidney Diseases; Male; Melanocyte-Stimulating Hormones; Mice; Neurosecretion; Organ Size; Pituitary Gland; Pituitary-Adrenal System; Stress, Physiological; Vasopressins

Topics: Adolescent; Adult; Chlorpropamide; Creatinine; Dehydration; Depression, Chemical; Diabetes Insipidus; Diuresis; Ethanol; Humans; Middle Aged; Osmolar Concentration; Potassium; Sodium; Urine; Vasopressins; Water; Water Deprivation

Topics: Animals; Dehydration; Glomerular Filtration Rate; Natriuresis; Osmolar Concentration; Pituitary Gland, Posterior; Potassium; Sheep; Vasopressins; Water-Electrolyte Balance

Topics: Anesthesia, General; Animals; Dehydration; Male; Microscopy, Electron; Neurosecretion; Neurosecretory Systems; Pituitary Gland, Posterior; Rats; Vasopressins

Topics: Aged; Chronic Disease; Dehydration; Female; Humans; Hydrochlorothiazide; Hypernatremia; Inflammation; Natriuresis; Pituitary Diseases; Pituitary Gland, Posterior; Sodium; Thirst; Vasopressins

Topics: Animals; Body Weight; Dehydration; Hypothalamo-Hypophyseal System; Male; Neurosecretion; Osmolar Concentration; Rats; Secretory Rate; Vasopressins; Water

Topics: Animals; Body Fluids; Dehydration; Pituitary Gland, Posterior; Rats; Vasopressins; Water

Topics: Animals; Chlorides; Dehydration; Female; Goats; Lactation; Lactose; Milk; Potassium; Pregnancy; Sodium; Vasopressins

Topics: Adenosine Triphosphatases; Aminohippuric Acids; Angiotensin II; Animals; Dehydration; In Vitro Techniques; Kidney Tubules; Ouabain; Perfusion; Rabbits; Sodium; Stimulation, Chemical; Vasopressins

Topics: Acid-Base Equilibrium; Animals; Dehydration; Diuresis; Dogs; Glomerular Filtration Rate; Humans; Kidney; Kidney Concentrating Ability; Kidney Tubules; Mannitol; Natriuresis; Osmosis; Potassium; Regional Blood Flow; Rheology; Sodium; Vasopressins; Water-Electrolyte Balance

1. The composition of renal tissue was determined in rats before and immediately after intravenous infusion of dextrose (2.5 g/100 ml.) in amounts sufficient to administer a positive fluid load of 4% body weight over 2 hr. The rats were classified into three groups, according to the preinfusion urine osmolality: hydropaenia, normal and moderately diuretic (over 2400, 800-1500 and below 800 mu-osmoles/g H(2)O, respectively).2. In non-infused rats, the steepness of the corticomedullary osmolal gradient varied, due to differences in both water and solute (sodium and urea) contents, and was related to urinary osmolality. Whereas differences in medullary and papillary solute contents occurred between all three groups, papillary water content was significantly higher only in the moderately diuretic animals.3. Dextrose infusion caused the induction of water diuresis, the lowest urinary osmolalities being produced in the previously moderately diuretic animals.4. Dextrose infusion caused a considerable reduction in the steepness of the corticomedullary osmolal gradient in all rats, particularly in the previously hydropaenic animals, due to changes in both solute (sodium and urea) and water contents. Whereas reductions in medullary and papillary solute contents occurred in all three groups, there was no further increase in papillary water content from the already high values seen in the noninfused diuretic animals.5. Thus, dextrose infusion largely abolished any previous differences in tissue water content, whereas significant, though small, differences in osmolal (particularly urea) content persisted.6. These data are discussed in terms of changes and differences in endogenous antidiuretic hormone (A.D.H.) release.7. Changes in the magnitude and direction of the urinary-papillary urea concentration difference are discussed in terms of passive transport, with probable A.D.H.-induced changes in nephron urea permeability.

Topics: Animals; Biological Transport; Dehydration; Diuresis; Glucose; Injections, Intravenous; Kidney; Male; Osmolar Concentration; Rats; Sodium; Urea; Urine; Vasopressins; Water

Topics: Animals; Dehydration; Diabetes Mellitus; Diabetes Mellitus, Experimental; Drinking; Insulin, Long-Acting; Male; Osmolar Concentration; Pancreatectomy; Pituitary Gland, Posterior; Plasma; Rats; Vasopressins; Water

Topics: Animals; Chlorpromazine; Dehydration; Diuresis; Male; Rats; Vasopressins

Topics: Adult; Angioedema; Biological Transport; Dehydration; Edema; Female; Humans; Kidney; Male; Psychophysiologic Disorders; Sodium; Stress, Psychological; Urea; Vasopressins

Topics: Animals; Dehydration; Hypothalamus; Oxytocin; Peptide Hydrolases; Rabbits; Vasopressins; Water Intoxication

Topics: Animals; Blood Urea Nitrogen; Calcium; Dehydration; Diabetes Insipidus; Female; Genes, Dominant; Hypothalamo-Hypophyseal System; Kidney; Kidney Concentrating Ability; Liver; Magnesium; Male; Mice; Muscles; Osmolar Concentration; Potassium; Sodium; Urine; Vasopressins

Topics: Adenine Nucleotides; Adenylyl Cyclases; Animals; Cyclic AMP; Dehydration; Kidney; Male; Phosphoric Monoester Hydrolases; Rats; Vasopressins; Water

Topics: Chlorpropamide; Creatinine; Cyclic AMP; Dehydration; Diuresis; Female; Humans; Hydrochlorothiazide; Hypernatremia; Hypothalamus; Insulin; Insulin Secretion; Islets of Langerhans; Kidney; Middle Aged; Osmolar Concentration; Sodium; Thirst; Tolbutamide; Vasopressins; Water; Water-Electrolyte Balance

Topics: Amphetamine; Animals; Body Weight; Dehydration; Guinea Pigs; Hematocrit; Hypothalamo-Hypophyseal System; Hypothalamus; Male; Pituitary Gland; Reserpine; Stimulation, Chemical; Sympathetic Nervous System; Synapses; Synaptic Transmission; Vasopressins; Water; Water Deprivation

Topics: Animals; Cell Nucleus; Cytoplasmic Granules; Dehydration; Diuresis; Female; Histological Techniques; Kidney; Lipid Metabolism; Prostaglandins; Rats; Statistics as Topic; Vasopressins

Topics: Adult; Blood Glucose; Dehydration; Diabetes Mellitus; Diabetic Coma; Diabetic Ketoacidosis; Diabetic Retinopathy; Glucose; Humans; Hyperglycemia; Hypothalamo-Hypophyseal System; Iatrogenic Disease; Insulin; Male; Pituitary Hormones, Anterior; Stress, Physiological; Vasopressins

Topics: Biopsy; Body Temperature; Body Weight; Brain Diseases; Calcium; Child; Child, Preschool; Chlorides; Creatine; Dehydration; Diabetes Insipidus; Diagnosis, Differential; Diet; Diuresis; Feeding and Eating Disorders; Female; Humans; Hydrochlorothiazide; Hypothalamus; Infant; Kidney; Male; Mineralocorticoid Receptor Antagonists; Obesity; Osmolar Concentration; Osmosis; Piperidines; Potassium; Sodium; Urography; Vasopressins

This study utilized rates with hereditary hypothalamic diabetes insipidus (D.I.) in order to explore possible mechanisms which prevent full urinary concentration after acute administration of vasopressin in hypothalamic D.I. and which correct this concentrating defect with prolonged therapy.IT WAS FOUND: (a) that the concentrating defect persisted even when the urinary osmolal excretion of D. I. rats was reduced to that of normal animals; (b) that the defect was not corrected more rapidly if larger doses of vasopressin were given; (c) that it persisted even when the D.I. rats were deprived of drinking water after vasopressin was given; (d) that there was osmotic equilibration between urine and renal papilla at a time when the concentrating defect was still evident; and (e) that the correction of the defect was associated with progressive and significant rise of the papillary osmolality. These studies appear to rule out osmotic diuresis, accumulation of exogenous vasopressin, persistent primary polydipsia, or delay in the induction of membrane permeability as causes for the concentrating defect. Rather, subnormal osmolality of the renal papilla, which can be corrected only gradually, accounts for the initial concentrating defect and the long time required for its correction. Reduction of water content and increase of urea content are primarily responsible for restoration of papillary osmolality to normal.

Topics: Animals; Dehydration; Diabetes Insipidus; Diuresis; Hypothalamus; Kidney; Kidney Concentrating Ability; Osmosis; Rats; Urea; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Blood Chemical Analysis; Body Weight; Dehydration; Hematocrit; Male; Osmolar Concentration; Oxytocin; Pituitary Gland; Rats; Vasopressins

Topics: Animals; Bromides; Dehydration; Diuresis; Ethylamines; Injections, Subcutaneous; Kidney; Kidney Concentrating Ability; Kidney Papillary Necrosis; Osmosis; Rats; Renal Veins; Vasopressins

Topics: Animals; Anura; Dehydration; Diuresis; Female; Hypophysectomy; Hypothalamus; Male; Sodium Chloride; Vasopressins; Water-Electrolyte Balance

Topics: Child; Dehydration; Female; Hormones; Humans; Hypernatremia; Hypothalamus; Pinealoma; Polyuria; Thirst; Vasopressins

1. With the aim of producing diabetes insipidus in sheep, electrolytic lesions were placed in the ventral medial hypothalamus immediately posterior to the optic chiasm.2. After formation of lesions, the pattern of urine excretion showed a triphasic response consisting of (i) an immediate diuresis reaching a maximum within 4 days, (ii) an interphase of about 12 days wherein rates of urine flow were normal, and (iii) a final phase of permanent polyuria. With the four sheep used in this work, the time between placement of the lesions and onset of permanent hyposthenuria was 19-22 days.3. In the final polyuric phase, the sheep were unable to concentrate their urine in response to dehydration or to feeding.4. Infusions of arginine vasopressin restored the ability of these animals to excrete urine that was hypertonic to plasma.5. The evidence showed that the hypothalamic lesions were effective in producing permanent diabetes insipidus. It was concluded that anti-diuretic hormone (ADH) has essentially the same function in sheep as it has in other mammalian species; that is, the hormone facilitates the elaboration of hypertonic urine. There was no evidence to suggest that ADH had a special effect on potassium excretion in the sheep.

Topics: Animals; Arginine; Dehydration; Diabetes Insipidus; Diet; Diuresis; Female; Hypothalamus; Kidney; Kidney Concentrating Ability; Osmosis; Osmotic Pressure; Polyuria; Potassium; Sheep; Time Factors; Urination; Vasopressins

Topics: Animals; Cell Nucleolus; Cell Nucleus; Dehydration; Hypothalamus; Lizards; Neurons; Neurosecretion; Osmotic Pressure; Vasopressins

Topics: Adrenal Glands; Animals; Dehydration; Diuresis; Drinking; Female; Histocytochemistry; Hypothalamo-Hypophyseal System; Male; Neurosecretion; Organ Size; Pituitary Gland, Posterior; Rats; Vasopressins; Water Deprivation

Topics: Adrenal Glands; Animals; Chickens; Dehydration; Female; Poultry Diseases; Starvation; Thyroid Gland; Thyroxine; Vasopressins

Topics: Adult; Arginine; Dehydration; Diuresis; Female; Humans; Kidney Tubules; Kinetics; Lysine; Male; Vasopressins

Topics: Animals; Dehydration; Electrophoresis; Neurosecretion; Organ Size; Oxytocin; Peptides; Pituitary Gland, Posterior; Rats; Sodium Chloride; Vasopressins

Topics: Adenosine Triphosphate; Animals; Dehydration; Ischemia; Kidney; Male; Rats; Vasopressins

Topics: Animals; Antidepressive Agents; Dehydration; Male; Monoamine Oxidase Inhibitors; Phenobarbital; Rats; Tranquilizing Agents; Urination; Vasopressins

Topics: Adenoma, Chromophobe; Chronic Disease; Dehydration; Diuresis; Humans; Hydrocortisone; Hypernatremia; Male; Mannitol; Middle Aged; Pituitary Gland, Posterior; Potassium; Sodium; Thirst; Vasopressins; Water-Electrolyte Balance

Topics: Adolescent; Adult; Blood Volume; Dehydration; Diabetes Insipidus; Female; Hematocrit; Humans; Hyperaldosteronism; Hypertension, Renal; Male; Renin; Sodium; Vasopressins; Water

Topics: Aminohippuric Acids; Animals; Biological Transport; Carbon Isotopes; Chlorides; Creatinine; Dehydration; Diuresis; Diuretics; Dogs; Female; Glomerular Filtration Rate; Glucose; Hemodynamics; Inulin; Kidney; Kidney Tubules; Mannitol; Nephrectomy; Osmosis; Sodium; Urea; Urination; Vasopressins; Water

Topics: Animals; Dehydration; Diabetes Insipidus; Diagnosis, Differential; Diuresis; Glomerular Filtration Rate; Humans; Hypernatremia; Hypothalamus; Kidney; Mammals; Physiology, Comparative; Polyuria; Thirst; Vasopressins; Water; Water-Electrolyte Balance

Topics: Adult; Animals; Biological Assay; Dehydration; Female; Humans; Hypertonic Solutions; Infusions, Parenteral; Injections, Intravenous; Male; Nicotine; Rats; Sodium Chloride; Vasopressins

Topics: Animals; Anura; Dehydration; Electrophoresis; Glycolates; Osmosis; Oxytocin; Pituitary Gland, Posterior; Pituitary Hormones, Posterior; Poultry; Reptiles; Sodium Chloride; Vasopressins

Topics: Adolescent; Adult; Animals; Biological Assay; Dehydration; Diabetes Insipidus; Diuresis; Female; Humans; Hypothalamus; Injections, Intravenous; Male; Rats; Vasopressins; Water

Topics: Animals; Dehydration; Diabetes Insipidus; Electrolytes; Kidney; Rats; Urea; Vasopressins

Topics: Animals; Coloring Agents; Dehydration; Diabetes Insipidus; Kidney; Microscopy, Fluorescence; Rats; Regional Blood Flow; Vasopressins

Topics: Animals; Dehydration; Diabetes Insipidus; Hypothalamus; In Vitro Techniques; Iodine Isotopes; Kidney; Liver; Rats; Thyroid Gland; Thyroxine; Vasopressins

Topics: Animals; Dehydration; Diabetes Insipidus; Hypothalamus; Potassium; Rats; Sodium; Starvation; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Absorption; Animals; Body Fluids; Dehydration; Dogs; Kinetics; Organomercury Compounds; Osmosis; Peritoneum; Vasopressins

Topics: Animals; Cats; Dehydration; Diabetes Insipidus; Diuresis; Hypothalamo-Hypophyseal System; Hypothalamus; Nicotine; Osmosis; Vasopressins; Water-Electrolyte Balance

Topics: Adolescent; Adult; Aminohippuric Acids; Blood Chemical Analysis; Creatine; Dehydration; Diuresis; Female; Humans; Hypertonic Solutions; In Vitro Techniques; Infusions, Parenteral; Male; Paraplegia; Polyuria; Quadriplegia; Vasopressins

Topics: Aged; Calcium; Coma; Dehydration; Humans; Magnesium; Potassium; Secretory Rate; Vasopressins; Water Intoxication; Water-Electrolyte Balance

Topics: Acetazolamide; Child; Dehydration; Diet Therapy; Humans; Hypernatremia; Hypothalamus; Male; Mercaptopurine; Potassium; Thirst; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Dehydration; Dietary Proteins; Kidney; Rats; Thirst; Vasopressins

Topics: Animals; Blood; Dehydration; Guinea Pigs; Hypothalamus; Pituitary Gland, Posterior; Vasopressins

Topics: Animals; Animals, Newborn; Dehydration; Diabetes Insipidus; Hydrocephalus; Hypothalamo-Hypophyseal System; Hypothalamus; Nerve Degeneration; Rats; Vasopressins

Topics: Adolescent; Adult; Aged; Animals; Dehydration; Diabetes Insipidus; Diuresis; Diuretics; Edema; Female; Humans; Hypertonic Solutions; Infusions, Parenteral; Liver Cirrhosis; Male; Middle Aged; Plasmacytoma; Rats; Urine; Vasopressins

Topics: Child; Dehydration; Drug Therapy; Humans; Hypernatremia; Hypothalamus; Hypothyroidism; Metabolism; Neoplasms; Neurosurgery; Pinealoma; Pituitary-Adrenal Function Tests; Prednisone; Thirst; Triiodothyronine; Vasopressins; Water-Electrolyte Balance

Topics: Adrenalectomy; Arginine Vasopressin; Dehydration; Dietary Proteins; Fasting; Kidney; Pharmacology; Rats; Research; Sodium; Sodium Chloride; Sodium, Dietary; Urine; Vasopressins; Water

The absorption of Thorotrast and saccharated iron oxide by the epithelium of the toad urinary bladder was studied by electron microscopy. Whether the toads were hydrated, dehydrated, or given Pitressin, no significant differences in transport of colloidal particles by epithelial cells were observed. This implies that these physiological factors had little effect on the transport of the tracer particles. Tracer particles were encountered in three types of epithelial cells which line the bladder lumen, but most frequently in the mitochondria-rich cells. Tracer materials were incorporated into the cytoplasm of epithelial cells after being adsorbed to the coating layer covering the luminal surface of the cells. In the intermediate stage (1 to 3 hours after introducing tracer) particles were present in small vesicles, tubules, and multivesicular bodies. In the later stages (up to 65 hours), the particles were more commonly seen to be densely packed within large membrane-bounded bodies which were often found near the Golgi region. These large bodies probably were formed by the fusion of small vesicles. Irrespective of the stages of absorption, no particles were found in the intercellular spaces or in the submucosa. Particles apparently did not penetrate the intercellular spaces of the epithelium beyond the level of the tight junction.

Topics: Absorption; Anura; Biological Transport; Cytoplasm; Dehydration; Electrons; Epithelial Cells; Epithelium; Golgi Apparatus; Iron; Microscopy; Microscopy, Electron; Mitochondria; Research; Thorium Dioxide; Urinary Bladder; Vasopressins

Topics: Animals, Newborn; Arginine Vasopressin; Blood; Chymotrypsin; Dehydration; Diuresis; Endocrinology; Inulin; Kidney Function Tests; Leucyl Aminopeptidase; Peptide Hydrolases; Physiology; Rats; Research; Trypsin; Vasopressins; Weaning

Topics: Adolescent; Anemia; Anemia, Sickle Cell; Black People; Body Weight; Child; Dehydration; Humans; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Body Fluids; Chemical Phenomena; Chemistry; Dehydration; Desert Climate; Diuresis; Humans; In Vitro Techniques; Kidney Function Tests; Mannitol; Urine; Vasopressins

Topics: Animals; Dehydration; Diuresis; Dogs; Kidney Function Tests; Mannitol; Osmosis; Research; Sodium; Urine; Vasopressins; Water

Topics: Dehydration; Diuresis; Electrons; Kidney; Kidney Glomerulus; Microscopy; Microscopy, Electron; Natriuresis; Osmosis; Pharmacology; Rats; Research; Sodium; Urea; Vasopressins

Topics: Arginine Vasopressin; Biological Assay; Blood Chemical Analysis; Blood Specimen Collection; Catheterization; Dehydration; Rats; Research; Urinary Catheterization; Vasopressins

Topics: Arginine Vasopressin; Dehydration; Diuresis; Diuretics; Glycosaminoglycans; Hexosamines; Histocytochemistry; Kidney; Pharmacology; Rats; Research; Vasopressins

Topics: Acute Kidney Injury; Atropine; Biomedical Research; Blood Volume; Convalescence; Dehydration; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Edema; Epinephrine; Female; Heart Failure; Hemorrhage; Humans; Hypertonic Solutions; Menstruation; Pharmacology; Placebos; Pregnancy; Renal Insufficiency; Salivation; Sweating; Uremia; Vasopressins; Water-Electrolyte Balance

Topics: Arginine Vasopressin; Dehydration; Kidney; Kidney Function Tests; Pharmacology; Rats; Research; Tannins; Vasopressins; Water Deprivation

Topics: Angiotensins; Aortic Diseases; Brain; Brain Damage, Chronic; Dehydration; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Hexamethonium Compounds; Humans; Infant; Infant, Newborn; Infant, Newborn, Diseases; Kidney Function Tests; Norepinephrine; Physiology; Renal Artery Obstruction; Vasopressins; Water-Electrolyte Balance

Topics: Ammonium Chloride; Arginine Vasopressin; Bicarbonates; Dehydration; Hypertonic Solutions; Kidney; Microchemistry; Pharmacology; Proteins; Rats; Research; Sodium Chloride; Sulfhydryl Compounds; Vasopressins

Topics: Dehydration; Fasting; Kidney; Kidney Concentrating Ability; Kidney Glomerulus; Natriuresis; Pharmacology; Physiology; Potassium; Rats; Research; Urine; Vasopressins

Topics: Arginine Vasopressin; Body Fluids; Dehydration; Homeostasis; Humans; Osmosis; Sleep; Smoking; Thirst; Urine; Vasopressins; Water

Topics: Blood Volume; Creatine; Creatinine; Dehydration; Diuresis; Dogs; Hemorrhage; Hypertonic Solutions; Kidney Tubules; Mannitol; Natriuresis; Osmosis; Pharmacology; Photometry; Potassium; Research; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Arginine Vasopressin; Blood; Chlorides; Dehydration; Diet; Dietary Proteins; Metabolism; Potassium; Potassium Chloride; Rats; Research; Sodium Chloride; Urea; Vasopressins

Topics: Arginine Vasopressin; Dehydration; Disulfides; Kidney; Kidney Tubules; Sulfhydryl Compounds; Vasopressins

Topics: Arginine Vasopressin; Dehydration; Diabetes Insipidus; Fetal Diseases; Humans; Hypernatremia; Infant; Infant Nutrition Disorders; Measles; Vasopressins

Topics: Animals; Arginine Vasopressin; Dehydration; Desoxycorticosterone; Desoxycorticosterone Acetate; Dextrans; Diuretics; Diuretics, Osmotic; Dogs; Mannitol; Research; Sodium Chloride; Surgical Procedures, Operative; Urea; Vasopressins

Topics: Adrenal Glands; Arginine Vasopressin; Blood Chemical Analysis; Blood Volume; Dehydration; Desoxycorticosterone; Methylprednisolone; Pharmacology; Physiology; Pituitary Gland; Pituitary Gland, Posterior; Rats; Research; Sodium; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Arginine Vasopressin; Dehydration; Humans; Pituitary Gland; Skin Physiological Phenomena; Vasopressins; Water

Topics: Arginine Vasopressin; Complementary Therapies; Dehydration; Humans; Urinary Tract Physiological Phenomena; Vasopressins

Topics: Arginine Vasopressin; Complementary Therapies; Dehydration; Humans; Urinary Tract Physiological Phenomena; Vasopressins

Topics: Animals; Arginine Vasopressin; Dehydration; Rats; Starvation; Thyroid Gland; Vasopressins

Topics: Animals; Arginine Vasopressin; Dehydration; Rats; Vasopressins; Water; Water Deprivation

Topics: Arginine Vasopressin; Body Fluids; Dehydration; Humans; Urine; Vasopressins

Topics: Arginine Vasopressin; Chlorides; Dehydration; Humans; Hyponatremia; Sodium; Sodium Chloride; Sweat; Sweating; Urine; Vasopressins

Topics: Animals; Dehydration; Hormones; Pituitary Gland; Pituitary Gland, Posterior; Rats; Urine; Vasopressins

Topics: Dehydration; Hormones; Humans; Neuroglia; Pituitary Gland; Pituitary Gland, Posterior; Vasopressins