pituitrin and Water-Electrolyte-Imbalance

The ability to regulate water movement is vital for the survival of cells and organisms. In addition to passively crossing lipid bilayers by diffusion, water transport is also driven across cell membranes by osmotic gradients through aquaporin water channels. There are 13 aquaporins in human tissues, and of these, aquaporin-2 (AQP2) is the most highly regulated water channel in the kidney: The expression and trafficking of AQP2 respond to body volume status and plasma osmolality via the antidiuretic hormone, vasopressin (VP). Dysfunctional VP signaling in renal epithelial cells contributes to disorders of water balance, and research initially focused on regulating the major cAMP/PKA pathway to normalize urine concentrating ability. With the discovery of novel and more complex signaling networks that regulate AQP2 trafficking, promising therapeutic targets have since been identified. Several strategies based on data from preclinical studies may ultimately translate to the care of patients with defective water homeostasis.

Topics: Animals; Aquaporin 2; Cell Membrane; Cyclic AMP; Cyclic AMP-Dependent Protein Kinases; Humans; Kidney; Neurophysins; Protein Precursors; Signal Transduction; Vasopressins; Water; Water-Electrolyte Balance; Water-Electrolyte Imbalance

ADH is a hormone secreted by neurohypophysis that plays different roles based on the target organ. At the renal level, this peptide is capable of causing electrolyte-free water absorption, thus playing a key role in the hydro-electrolytic balance. There are pathologies and disorders that jeopardize this balance and, in this field, ADH receptor inhibitors such as Vaptans could play a key role. By inhibiting the activation pathway of vasopressin, they are potentially useful in euvolemic and hypervolemic hypotonic hyponatremia. However, clinical trials in heart failure have not given favourable results on clinical outcomes. Even in SIADH, despite their wide use, there is no agreement by experts on their use. Since vaptans inhibit the cAMP pathway in tubular cells, their use has been proposed to inhibit cystogenesis. A clinical trial has shown favourable effects on ADPKD progression. Because vaptans have been shown to be effective in models of renal cysts disorders other than ADPKD, their use has been proposed in diseases such as nephronophthisis and recessive autosomal polycystic disease. Other possible uses of vaptans could be in kidney transplantation and cardiorenal syndrome. Due to the activity of ADH in coagulation and haemostasis, ADH's activation pathway by Desmopressin Acetate could be a useful strategy to reduce the risk of bleeding in biopsies in patients with haemorrhagic risk.

Topics: Antidiuretic Hormone Receptor Antagonists; Cadaver; Cyclic AMP; Forecasting; Humans; Hyponatremia; Kidney Diseases; Kidney Diseases, Cystic; Kidney Transplantation; Kidney Tubules, Collecting; Molecular Targeted Therapy; Neurophysins; Polycystic Kidney, Autosomal Dominant; Protein Precursors; Receptors, Vasopressin; Second Messenger Systems; Tissue Donors; Vasopressins; Water-Electrolyte Imbalance

Topics: Aquaporin 2; Biomarkers; Body Water; Diabetes Insipidus, Neurogenic; Education, Medical, Continuing; Humans; Inappropriate ADH Syndrome; Kidney; Polymers; Receptors, Vasopressin; Sodium; Vasopressins; Water-Electrolyte Imbalance

Disorders of body fluids are among the most commonly encountered problems in the practice of clinical medicine. This is in large part because many different disease states can potentially disrupt the finely balanced mechanisms that control the intake and output of water and solute. It therefore behooves clinicians treating such patients to have a good understanding of the pathophysiology, the differential diagnosis and the management of these disorders. Since body water is the primary determinant of the osmolality of the extracellular fluid (ECF), disorders of body water homeostasis can be divided into hypoosmolar disorders, in which there is an excess of body water relative to body solute, and hyperosmolar disorders, in which there is a deficiency of body water relative to body solute. The classical hyperosmolar disorder is diabetes insipidus (DI), and the classical hypoosmolar disorder is the syndrome of inappropriate antidiuretic hormone secretion (SIADH). This chapter first reviews the regulatory mechanisms underlying water and sodium metabolism, the two major determinants of body fluid homeostasis. The major disorders of water metabolism causing hyperosmolality and hypoosmolality, DI and SIADH, are then discussed in detail, including the pathogenesis, differential diagnosis and treatment of these disorders.

Topics: Animals; Diabetes Insipidus; Diagnosis, Differential; Humans; Hypernatremia; Inappropriate ADH Syndrome; Vasopressins; Water; Water-Electrolyte Imbalance

Dysnatremia is among the most common electrolyte disorders in clinical medicine and its improper management can have serious consequences associated with increased morbidity and mortality of patients. The aim of this study is to update the pathophysiology of dysnatremia and review some simple clinical and laboratory tools, easy to interpret, that allow us to make a quick and simple approach. Dysnatremia involves water balance disorders. Water balance is directly related to osmoregulation. There are mechanisms to maintain plasma osmolality control; which are triggered by 1-2% changes. Hypothalamic osmoreceptors detect changes in plasma osmolality, regulating the secretion of Antidiuretic Hormone (ADH), which travels to the kidneys resulting in more water being reabsorbed into the blood; therefore, the kidney is the main regulator of water balance. When a patient is suffering dysnatremia, it is important to assess how his ADH-renal axis is working. There are causes of this condition easy to identify, however, to differentiate a syndrome of inappropriate ADH secretion from cerebral salt-wasting syndrome is often more difficult. In the case of hypernatremia, to suspect insipidus diabetes and to differentiate its either central or nephrogenic origin is essential for its management. In conclusion, dysnatremia management requires pathophysiologic knowledge of its development in order to make an accurate diagnosis and appropriate treatment, avoiding errors that may endanger the health of our patients.

Topics: Child; Humans; Hypernatremia; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins; Water-Electrolyte Imbalance

Intravenous maintenance fluid therapy aims to replace daily urinary and insensible losses for ill children in whom adequate enteric administration of fluids is contraindicated or infeasible. The traditional determination of fluid volumes and composition dates back to Holliday and Segar's seminal article from 1957, which describes the relationship between weight, energy expenditure, and physiologic losses in healthy children. Combined with estimates of daily electrolyte requirements, this information supports the use of the hypotonic maintenance fluids that were widely used in pediatric medicine. However, using hypotonic intravenous fluids in a contemporary hospitalized patient who may have complex physiologic derangements, less caloric expenditure, decreased urinary output, and elevated antidiuretic hormone levels is often not optimal; evidence over the last 2 decades shows that it may lead to an increased incidence of hyponatremia. In this review, we present the evidence for using isotonic rather than hypotonic fluids as intravenous maintenance fluid.

Topics: Body Water; Child; Critical Care; Critical Illness; Disease Management; Diuresis; Elective Surgical Procedures; Electrolytes; Energy Metabolism; Fluid Therapy; Humans; Hyponatremia; Hypotonic Solutions; Infusions, Intravenous; Isotonic Solutions; Postoperative Care; Randomized Controlled Trials as Topic; Vasopressins; Water-Electrolyte Imbalance

Aquaporin-2 (AQP2), the vasopressin-regulated water channel of the renal collecting duct, is dysregulated in numerous disorders of water balance in people and animals, including those associated with polyuria (urinary tract obstruction, hypokalemia, inflammation, and lithium toxicity) and with dilutional hyponatremia (syndrome of inappropriate antidiuresis, congestive heart failure, cirrhosis). Normal regulation of AQP2 by vasopressin involves 2 independent regulatory mechanisms: (1) short-term regulation of AQP2 trafficking to and from the apical plasma membrane, and (2) long-term regulation of the total abundance of the AQP2 protein in the cells. Most disorders of water balance are the result of dysregulation of processes that regulate the total abundance of AQP2 in collecting duct cells. In general, the level of AQP2 in a collecting duct cell is determined by a balance between production via translation of AQP2 mRNA and removal via degradation or secretion into the urine in exosomes. AQP2 abundance increases in response to vasopressin chiefly due to increased translation subsequent to increases in AQP2 mRNA. Vasopressin-mediated regulation of AQP2 gene transcription is poorly understood, although several transcription factor-binding elements in the 5' flanking region of the AQP2 gene have been identified, and candidate transcription factors corresponding to these elements have been discovered in proteomics studies. Here, we review progress in this area and discuss elements of vasopressin signaling in the collecting duct that may impinge on regulation of AQP2 in health and in the context of examples of polyuric diseases.

Topics: Animals; Aquaporin 2; Humans; Kidney Tubules, Collecting; Polyuria; Signal Transduction; Vasopressins; Water-Electrolyte Imbalance

Diabetes insipidus (DI) is a rare disorder of horses characterized by profound polyuria and polydipsia (PU/PD), which can be caused by loss of production of arginine vasopressin (AVP). This condition is termed neurogenic or central DI. DI may also develop with absence or loss of AVP receptors or activity on the basolateral membrane of collecting-duct epithelial cells. This condition is termed nephrogenic DI. Equine clinicians may differentiate true DI from more common causes of PU/PD by a systematic diagnostic approach. DI may not be a correctable disorder, and supportive care of affected horses requires an adequate water source.

Topics: Animals; Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Female; Homeostasis; Horse Diseases; Horses; Male; Vasopressins; Water; Water-Electrolyte Imbalance

Anorexia nervosa (AN) is a serious eating disorder associated with numerous medical complications, including alterations in water balance and impaired osmoregulation.. The aim of this paper is to review the evidence-based literature and discuss the potential pathophysiological mechanisms of impaired osmoregulation observed in patients with AN.. Although limited, the evidence suggests that the pathophysiological mechanisms causing impaired osmoregulation in AN is multifactorial and includes abnormalities in osmoregulation of vasopressin, intrinsic renal defects and the influence of antidepressants often used in the treatment of patients with AN. Physicians treating patients with AN should be aware of this complication and the possible multifactorial etiology contributing to this medical complication.

Topics: Adolescent; Anorexia Nervosa; Antidepressive Agents; Evidence-Based Medicine; Humans; Kidney; Kidney Failure, Chronic; Vasopressins; Water-Electrolyte Imbalance

Endolymph homeostasis is thought to be mediated by the vasopressin-aquaporin-2 (VP-AQP2) system in the inner ear. Endolymphatic hydrops, the morphological characteristics of Ménière's disease (MD), seems to reflect the malregulation of the VP-AQP2 system in inner ear fluid. The elevation of plasma vasopressin (p-VP) level, which is often observed in MD and its related diseases, might be one of the causative factors underlying these diseases.. Review of the role of the VP-AQP2 system in the inner ear fluid homeostasis and in the formation and development of endolymphatic hydrops.. A clinical survey has revealed that the p-VP level is often elevated in MD and its related diseases and that the increase in the p-VP level was closely linked to vertigo attacks in MD. Experimental studies have revealed that proteins and mRNAs of aquaporin-2 and vasopressin type 2 receptor were expressed in the stria vascularis of the cochlea and the epithelium of the endolymphatic sac, and that the volume of the endolymphatic compartment was mediated by the activity of the VP-AQP2 system in the inner ear.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Aquaporin 2; Benzazepines; Diuretics; Ear, Inner; Endolymph; Homeostasis; Humans; Lithium; Meniere Disease; Vasopressins; Water-Electrolyte Imbalance

Topics: Animals; Aquaporin 2; Aquaporins; Endocytosis; Exocytosis; Heart Failure; Humans; Kidney; Kidney Concentrating Ability; Liver Cirrhosis; Phosphorylation; Protein Transport; Signal Transduction; Urologic Diseases; Vasopressins; Water; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Intensive care patients often suffer from hypo- or hypernatremia. These dysnatremias reflect an antidiuretic-hormone (ADH)-related water imbalance and are the result of the underlying disease. However, they are often triggered by drug side effects and exacerbated by an intentional or unintentional sodium imbalance. Dysnatremias are also caused by artificial ventilation; however, the mechanisms behind this are beyond the scope of this article. Considerations regarding etiology, water and sodium balance and, in particular, the variable in urine dilution or concentration, take priority over a brisk normalization of sodium concentration. Therefore, the 3 most important factors are: 1) delivery of water and sodium to the collecting duct; 2) generation and maintenance of an osmotic pressure gradient exerted by solutes present in the renal medullary interstitium; 3) the regulated water permeability of collecting duct cells under the control of antidiuretic hormone. With these, most disorders can already be identified from patient history and simple factors such as body weight and serum and urine osmolality.

Topics: Critical Care; Diabetes Insipidus; Humans; Inappropriate ADH Syndrome; Sodium; Vasopressins; Water-Electrolyte Imbalance

Copeptin denominates the C-terminal fragment of the vasopressin (AVP) precursor hormone. Circulating copeptin levels reflect the activity of the AVP system and correlate closely with plasma osmolality. The measurement of stimulated plasma AVP levels is crucial in the differential diagnosis of diabetes insipidus, particularly the characterization of partial forms, and is used to diagnose primary polydipsia. However, determination of AVP levels is technically demanding, and validated assays are not readily available for clinical routine. Recently, a reliable sandwich immunoassay for measurement of serum or plasma copeptin levels has been introduced. Assaying stimulated copeptin levels will be helpful in the differential diagnosis of diabetes insipidus. Recent studies suggest that measurement of copeptin, once the assay is commercially available, might prove useful in the workup of hyponatremic disorders. Moreover, copeptin has been found to be a prognostically relevant biomarker in a variety of illnesses such as sepsis, shock, pneumonia, acute exacerbation of COPD, heart failure, and myocardial infarction.

Topics: Biomarkers; Diabetes Insipidus; Glycopeptides; Humans; Hyponatremia; Immunoassay; Prognosis; Protein Precursors; Vasopressins; Water-Electrolyte Imbalance

Vasopressin analogues are increasingly used for haemodynamic support of catecholamine-refractory, hyperdynamic septic shock. Arginine vasopressin (AVP) and terlipressin (TP) effectively increase mean arterial pressure and reduce catecholamine requirements in this condition. However, the use of either of the drugs may be linked to relevant haemodynamic side effects, including reductions in cardiac output, oxygen delivery and mixed-venous oxygen saturation. These alterations may result in impaired tissue perfusion and foster the genesis of ischemic tissue injury. In addition, decreases in platelet count and increases in aminotransferases activity and bilirubin concentration have been reported with the use of V1 agonists. However, it remains unclear whether these changes are of clinical relevance. This review article summarizes the previous data on adverse effects related to the therapy with vasopressin analogues and discusses potential options to prevent such adverse events. In summary, continuous TP infusion appears to be superior to bolus infusion. Maximum doses of 0.03 (-0.067) U min(-1) of AVP or 2 microg kg(-1) h(-1) of TP, respectively, should not be exceeded. Aggressive fluid therapy may prevent adverse haemodynamic effects linked to infusion of either AVP or TP. Finally, platelet count, surrogate variables of hepatic dysfunction, electrolytes and osmolality should be strictly monitored in patients treated with vasopressin analogues.

Topics: Animals; Chemical and Drug Induced Liver Injury; Humans; Ischemia; Kidney Diseases; Lypressin; Shock; Skin; Terlipressin; Thrombosis; Vasoconstrictor Agents; Vasopressins; Water-Electrolyte Imbalance

Hyponatremia is the most common electrolyte disorder present in hospitalized patients. Acute and severe hyponatremia can cause significant morbidity and mortality. The present review discusses the epidemiology, causes, and a practical approach to the diagnosis and management of acute and chronic hyponatremia, including the appropriate use of hypertonic saline and potential future use of the new V2 vasopressin receptor antagonists in critically ill patients.. The increasing knowledge of aquaporin water channels and the role of vasopressin in water homeostasis have enhanced our understanding of hyponatremic disorders. Increased vasopressin secretion due to nonosmotic stimuli leads to decreased electrolyte-free water excretion with resulting water retention and hyponatremia. Vasopressin receptor antagonists induce electrolyte-free water diuresis without natriuresis and kaliuresis. Phase three trials indicate that these agents predictably reduce urine osmolality, increase electrolyte-free water excretion, and raise serum sodium concentration. They are likely to become a mainstay of treatment of euvolemic and hypervolemic hyponatremia.. The correct diagnosis and management of hyponatremia is complex and requires a systematic approach. Vasopressin receptor antagonists are potential tools in the management of hyponatremia. Further studies are needed to determine their role in the treatment of acute, severe, life-threatening hyponatremia as well as chronic hyponatremia.

Topics: Acute Disease; Humans; Hyponatremia; Osmolar Concentration; Osmotic Pressure; Receptors, Vasopressin; Vasoconstrictor Agents; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Disorders of water balance are a common feature of clinical practice. An understanding of the physiology and pathophysiology of the key endocrine regulator of water balance vasopressin (VP) is key to diagnosis and management of these disorders. Diabetes insipidus is the result of a lack of VP or (less commonly) resistance to the renal effects of the hormone. Diagnostic testing can clarify aetiology and direct appropriate management. VP production can be associated with hyponatraemia. A comprehensive assessment of cardiovascular status and pharmacological influences are needed in these circumstances to differentiate between primary (inappropriate) and secondary (appropriate) physiological VP production. As with diabetes insipidus, diagnostic testing can help define the aetiology of hyponatraemia and direct appropriate management. Patients with disorders of water balance benefit from a joint clinical and laboratory medicine approach to diagnosis and management.

Topics: Aquaporins; Body Water; Diabetes Insipidus; Diuresis; Humans; Hypernatremia; Hyponatremia; Kidney; Molecular Structure; Polyuria; Receptors, Vasopressin; Sodium; Thirst; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Hyponatremia is frequently associated with neurological disease, neurosurgical procedures, and use of psychoactive drugs. Arginine vasopressin (AVP), or antidiuretic hormone, is the principal physiological regulator of water and electrolyte balance, and disruption of the normal AVP response to osmotic stimuli is a common cause of dilutional hyponatremia in neurological disorders. The hyponatremia-induced shift in water from the extracellular to the intracellular compartment can lead to cerebral edema and serious neurological complications, especially if the decrease in serum sodium concentration ([Na+]) is large or rapid. Overly rapid correction of the serum [Na+] may lead to osmotic demyelination and irreversible brain injury. Fluid restriction is considered first-line treatment and pharmacological agents currently used in the treatment of hyponatremia are limited by inconsistent response and adverse side effects. AVP receptor antagonists represent a new approach to the treatment of hyponatremia by blocking tubular reabsorption of water by binding to V2 receptors in the renal collecting ducts, resulting in aquaresis. Initial clinical experience with AVP receptor antagonists for hyponatremia has shown that these agents augment free water clearance, decrease urine osmolality, and correct serum [Na+] and serum osmolality. Controlled clinical trials now underway will help elucidate the role of AVP receptor antagonism in the treatment of hyponatremia.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Humans; Hyponatremia; Models, Biological; Nervous System Diseases; Osmolar Concentration; Receptors, Vasopressin; Sodium; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Pre-operative central diabetes insipidus has been reported in 8-35% of patients affected with craniopharyngioma, and in 70-90% after surgery. The management of postoperative polyuria and polydipsia can be challenging and fluid balance needs to be closely monitored. The classical triphasic pattern of endogenous vasopressin secretion--an initial phase of symptomatic diabetes insipidus occurring 24 hours after surgery; a second phase of inappropriate vasopressin secretion potentially causing hyponatraemia; and a third phase with a return to diabetes insipidus occurring up to 2 weeks later--is often complicated by cerebral salt wasting and thirst disorders. Inadequate adrenal replacement therapy and anticonvulsant agent treatment may increase the risk of life-threatening hyponatraemia in the course of desmopressin (DDAVP) treatment. Appropriate management, in order to avoid life-threatening or disabling electrolyte disturbances, requires a good grasp of the relevant pathophysiology. We review here the pathophysiology and management of the multiple fluid disorders encountered following surgery for craniopharyngiomas.

Topics: Child; Craniopharyngioma; Diabetes Insipidus; Humans; Hyponatremia; Neurosurgical Procedures; Pituitary Neoplasms; Postoperative Complications; Thirst; Vasopressins; Water-Electrolyte Imbalance

Topics: Body Water; Diabetes Insipidus; Electrolytes; Humans; Hyperaldosteronism; Hypertension; Hypoaldosteronism; Inappropriate ADH Syndrome; Natriuretic Peptides; Renin-Angiotensin System; Vasopressins; Water-Electrolyte Imbalance

Effects of vasopressin via V1a- and V2-receptors are closely implicated in a variety of water-retaining diseases and cardiovascular diseases, including heart failure, hyponatraemia, hypertension, renal diseases, syndrome of inappropriate antidiuretic hormone secretion, cirrhosis and ocular hypertension. As vasopressin receptors are found in many different tissues, vasopressin antagonists may benefit the treatment of disorders such as cerebral ischaemia and stroke, Raynaud's disease, dysmenorrhoea and tocolytic treatment. V1b selective vasopressin antagonists are discussed in terms of their usefulness in the treatment of emotional and psychiatric disorders. The vaptans are vasopressin receptor antagonists with V1a (relcovaptan) or V2 (tolvaptan, lixivaptan) selectivity or non-selective activity (conivaptan) which may be advantageous in some disorders. The V1a/V2 non-selective vasopressin antagonist conivaptan is the first vaptan which is approved by the FDA for the treatment of euvolaemic hyponatraemia.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Azepines; Benzamides; Benzazepines; Binding Sites; Cardiovascular Diseases; Clinical Trials as Topic; Hormone Antagonists; Humans; Indoles; Pyrroles; Pyrrolidines; Tolvaptan; Vasopressins; Water-Electrolyte Imbalance

Nocturia is common in older people and it may be bothersome for both patients and carers. It is most commonly related to bladder storage difficulties and nocturnal polyuria. The former results most frequently from an uninhibited overactive bladder. The latter occurs as a consequence of age-associated changes in the circadian rhythm of urine excretion. The management of an overactive bladder includes both behavioural and drug treatment. The management options for nocturnal polyuria include an afternoon diuretic and desmopressin, but caution is required, particularly with the latter, as it can cause significant hyponatraemia.

Topics: Adult; Aged; Aged, 80 and over; Arginine Vasopressin; Atrial Natriuretic Factor; Circadian Rhythm; Humans; Kidney Diseases; Life Style; Male; Middle Aged; Sleep Wake Disorders; Sodium; Urinary Bladder Diseases; Urination Disorders; Vasopressins; Water-Electrolyte Imbalance

Polyuria and polydipsia (PUPD) occur frequently in dogs and may be caused by a variety of endocrine, metabolic, and renal disturbances. The studies described in this PhD Thesis, which was defended in January 2004 in Utrecht, investigated the role of the antidiuretic hormone vasopressin (VP) in the pathogenesis of different forms of canine polyuria. Experiments in healthy dogs demonstrated that the ranges of urine specific gravity and urine osmolality are much larger than previously thought. A water deprivation test is not required in all polyuric dogs, because serial measurements of urine osmolality may already lead to the diagnosis of primary polydipsia, in some cases. In dogs with primary polydipsia a wide variation in VP responses to hypertonic stimulation can be found, including a hyperresponse, a hyporesponse, and a non-linear response. The significance of the VP response to hypertonic saline infusion as the 'gold standard' for a diagnosis of canine polyuria is discussed. In the dog, VP is secreted in a pulsatile fashion with a wide variation in the number of VP pulses, VP pulse duration, and VP pulse amplitude and height. The occurrence of spontaneous VP pulses may severely hamper the interpretation of the curve describing the relationship between plasma osmolality and plasma VP concentration during osmotic stimulation. A radioimmunoassay to measure the VP-dependent water channel aquaporin-2 (AQP2) in urine was developed in dogs. In healthy dogs, urinary AQP2 excretion closely reflects changes in collecting duct exposure to VP. Measurement of urinary AQP2 excretion in polyuric dogs may be helpful to distinguish between central diabetes insipidus, nephrogenic diabetes insipidus, and primary polydipsia.

Topics: Animals; Area Under Curve; Diagnosis, Differential; Dog Diseases; Dogs; Osmolar Concentration; Periodicity; Polyuria; Radioimmunoassay; Vasopressins; Water-Electrolyte Imbalance

Topics: Blood Pressure; Body Water; Electrolytes; Humans; Kidney Concentrating Ability; Osmotic Pressure; Plasma Volume; Thirst; Vasopressins; Water Loss, Insensible; Water-Electrolyte Imbalance

Osmotic demyelination of the brain (ODS) is a dreaded complication that typically occurs several days after aggressive therapy for chronic hyponatraemia, but is eminently avoidable. In this teaching exercise, Professor McCance, an imaginary consultant, is asked to explain how he would have treated a 28-year-old female who had hyperkalaemia, hypoglycaemia, hypotension and hyponatraemia (118 mM) to prevent the development of ODS. He begins with a review of the physiology, including his own landmark work on chronic hyponatraemia associated with a contracted extracellular fluid volume. Adding quantitative analysis, the cause of the excessive rise in plasma sodium concentration is revealed, and a better plan for therapy is proposed.

Topics: Addison Disease; Adult; Brain Diseases; Demyelinating Diseases; Female; Humans; Hyperkalemia; Hypoglycemia; Hyponatremia; Hypotension; Renal Agents; Syndrome; Vasopressins; Water-Electrolyte Imbalance

Hyponatremia, defined as a serum sodium < 135 mmol/l, is one of the most commonly encountered and serious electrolyte disorders of clinical medicine. The predominant cause of hyponatremia is an inappropriate elevation of circulating vasopressin levels relative to serum osmolality or the 'syndrome of inappropriate antidiuretic hormone secretion' (SIADH). Fortunately, the degree of the hyponatremia is limited by a process that counters the water-retaining action of vasopressin, namely 'vasopressin escape'. Vasopressin escape is characterized by a sudden increase in urine volume with a decrease in urine osmolality independent of circulating vasopressin levels. Until recently, little was known about the molecular mechanisms underlying escape. In the 1980s, we developed an animal model for vasopressin escape in which male Sprague-Dawley rats were infused with dDAVP, a V2-receptor-selective agonist of vasopressin, while being fed a liquid diet. Rats drank a lot of water in order to get the calories they desired. Using this model, we demonstrated that the onset of vasopressin escape (increased urine volume coupled to decreased urine osmolality) coincided temporally with a marked decrease in renal aquaporin-2 (water channel) protein and mRNA expression in renal collecting ducts. This protein reduction was reversible and correlated to decreased water permeability of the collecting duct. Studies examining the mechanisms underlying AQP2 decrease revealed a decrease in V2-receptor mRNA expression and binding, as well as a decrease in cyclic AMP production in response to acute-dDAVP challenge in collecting duct suspensions from these escape animals. Additional studies showed an increase in sodium transporters of the distal tubule. These changes, hypothetically, might help to attenuate the hyponatremia. Future studies are needed to fully elucidate systemic, intra-organ, and cellular signaling responsible for the physiological phenomenon of vasopressin escape.

Topics: Animals; Aquaporins; Carrier Proteins; Deamino Arginine Vasopressin; Diuresis; Kidney; Natriuresis; Rats; Vasopressins; Water-Electrolyte Imbalance

The hepatorenal syndrome is a form of renal failure occurring in patients with advanced liver disease. The diagnosis is based both on the demonstration of low GFR and exclusion of other common causes of renal failure that may occur in patients with cirrhosis. Orthotopic liver transplantation remains the only curative treatment for this poor outcome disease; other modalities such as vasopressin analogues, transjugular intrahepatic portosystemic shunt or renal replacement therapies may serve as a bridge to transplantation. This article reviews the pathophysiology, diagnosis and current treatment of hepatorenal syndrome.

Topics: Acute Kidney Injury; Creatinine; Diagnosis, Differential; Edema; Glomerular Filtration Rate; Hepatorenal Syndrome; Humans; Liver Cirrhosis; Liver Transplantation; Peritoneovenous Shunt; Portasystemic Shunt, Surgical; Renal Circulation; Renal Replacement Therapy; Renin-Angiotensin System; Serum Albumin; Splanchnic Circulation; Vasoconstrictor Agents; Vasodilator Agents; Vasopressins; Water-Electrolyte Imbalance

Topics: Animals; Aquaporins; Body Water; Carbon Tetrachloride Poisoning; Carrier Proteins; Ion Transport; Kidney Tubules, Proximal; Liver Cirrhosis, Experimental; Loop of Henle; Rats; Sodium; Sodium Channels; Structure-Activity Relationship; Vasopressins; Water-Electrolyte Imbalance

Topics: Diabetes Insipidus; Diagnosis, Differential; Diuretics; Humans; Inappropriate ADH Syndrome; Vasopressins; Water-Electrolyte Imbalance

The changes in sodium homeostasis most frequently are expression of water-electrolyte balance disturbances in patients with liver cirrhosis. Hyponatremia of water excess is found in 35% of the patients with cirrhosis and ascites. This disturbance is most frequently connected with raised antidiuretic hormone (vasopressin) secretion and is realized by including of nonosmotic stimulating mechanisms. The vasopressin plays a leading role in pathogenesis of disturbed water metabolism in the liver cirrhosis. Some patients with hepatorenal syndrome are established with highest plasma vasopressin concentrations. Gene expression of the regulation of kidney vasopressin-sensitive water channels (aquaporin-2 proteins) is also raised in the liver cirrhosis. Using in practice vasopressin-type 2 (V-2) receptor antagonists gives hopeful results in medical treatment of water-electrolyte disturbances in patients with advanced liver cirrhosis.

Topics: Gene Expression; Humans; Hyponatremia; Liver Cirrhosis; Renal Insufficiency; Sodium; Vasopressins; Water-Electrolyte Imbalance

The elderly are at increased risk of changes in body water and sodium, often accompanying comorbid disease states, which are associated with increased mortality. The clinical assessment of the hydration status of an elderly patient is difficult and the elderly care physician relies on both the clinical picture and laboratory investigation. Although still contentious, research suggests that the elderly may appreciate thirst less readily. However, healthy elderly may be able to produce an enhanced vasopressin response to osmotic stimulation compared to their younger counterparts, possibly in response to reduced renal function. The changes in these systems, when combined with coincident disease, place elderly patients at risk of water imbalance and electrolyte disturbance.

Topics: Aged; Aging; Humans; Middle Aged; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

The aquaporins are a recently recognized family of water channels that mediate water transport in kidney and in other organs. Aquaporin-2, 'vasopressin-regulated water channel', is regulated by vasopressin in two ways to account for overall control of collecting duct water permeability. First, vasopressin has a short-term effect in triggering translocation of aquaporin-2-containing intracytoplasmic vesicles to the apical plasma membrane, thus increasing principal cell water permeability. Second, vasopressin has a long-term effect in increasing the abundance of aquaporin-2 in collecting duct principal cells, increasing the maximal attainable water permeability. Using animal models, defects in these control mechanisms have been shown to be associated with several disorders of water balance, including central diabetes insipidus, congenital nephrogenic diabetes insipidus, acquired diabetes insipidus, syndrome of inappropriate antidiuretic hormone secretion, and several extracellular fluid volume expanded states.

Topics: Animals; Aquaporin 2; Aquaporin 6; Aquaporins; Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Drinking; Extracellular Space; Humans; Inappropriate ADH Syndrome; Ion Channels; Kidney Tubules, Collecting; Vasopressins; Water-Electrolyte Imbalance

Topics: Adrenomedullin; Angiotensin II; Animals; Atrial Natriuretic Factor; Endothelins; Glomerular Filtration Rate; Humans; Kidney Tubules, Proximal; Natriuresis; Nitrous Oxide; Peptides; Renal Circulation; Vasopressins; Water-Electrolyte Imbalance

Topics: Age Factors; Aged; Aged, 80 and over; Body Water; Edema; Female; Homeostasis; Humans; Hyponatremia; Kidney Tubules; Male; Osmolar Concentration; Risk Factors; Sodium; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Topics: Aging; Animals; Child; Diabetes Insipidus; Female; Humans; Male; Mutation; Pituitary Gland, Posterior; Receptors, Vasopressin; Vasopressins; Water-Electrolyte Imbalance

The delicate interplay between vasoconstrictors and vasodilators preserves glomerular filtration in CHF despite marked hypoperfusion. Activation of vasoconstrictive systems seems to depend on the severity and the chronicity of the disease. The importance of renin-angiotensin, sympathetic nerves, vasopressin and counterregulatory ANP, and prostaglandins in CHF has been elucidated. Possible roles of newly identified substances, such as endothelin and EDRF, deserve investigation.

Topics: Animals; Atrial Natriuretic Factor; Dogs; Dopamine; Endothelins; Heart Failure; Kidney; Natriuretic Peptide, Brain; Nerve Tissue Proteins; Nitric Oxide; Prostaglandins; Rats; Renin-Angiotensin System; Sympathetic Nervous System; Vasopressins; Water-Electrolyte Imbalance

Topics: Animals; Atrial Natriuretic Factor; Heart Failure; Humans; Kidney Tubules; Neurotransmitter Agents; Prostaglandins; Renin-Angiotensin System; Signal Transduction; Vasopressins; Water-Electrolyte Imbalance

Topics: Adolescent; Adult; Age Factors; Aged; Aged, 80 and over; Child; Child, Preschool; Female; Humans; Hypernatremia; Hyponatremia; Infant; Male; Middle Aged; Renin-Angiotensin System; Sodium; Vasopressins; Water-Electrolyte Imbalance

The acute effect of ethyl alcohol ingestion is to induce diuresis with excretion of free water and preservation of electrolytes. This occurs as the blood alcohol concentration is increasing and is due to the suppression by alcohol of the endogenous release of ADH. During a steady blood alcohol concentration, alcohol acts as an antidiuretic, causing retention of water and electrolytes. While at steady state, additional doses of alcohol will produce progressively smaller and eventually absent diuretic responses. The chronic effect of alcohol is to promote isosmotic retention of water and electrolytes due to increased ADH levels. Excess water and electrolytes are acutely excreted in response to additional alcohol ingestion. With the cessation of alcohol intake, this excess will be excreted over several days. Routine parenteral fluid administration to chronic and withdrawing alcoholics should be avoided. The role of potassium and magnesium in the genesis of specific manifestations of the alcohol withdrawal syndrome is not clear. Alcoholic patients may have electrolyte abnormalities due to alcohol-induced diseases, poor nutrition, or vomiting and diarrhea. Each case must be individually evaluated.

Topics: Alcoholism; Electrolytes; Emergency Medicine; Ethanol; Hemodynamics; Humans; Magnesium; Substance Withdrawal Syndrome; Vasopressins; Water-Electrolyte Imbalance

Topics: Diagnosis, Differential; Humans; Inappropriate ADH Syndrome; Vasopressins; Water-Electrolyte Imbalance

Topics: Animals; Brain; Cardiovascular System; Diabetes Insipidus; Humans; Oropharynx; Osmolar Concentration; Postoperative Complications; Vasopressins; Water-Electrolyte Imbalance

Topics: Atrial Natriuretic Factor; Humans; Hyperaldosteronism; Hypertension; Natriuresis; Sodium, Dietary; Vasopressins; Water-Electrolyte Imbalance

Disorders of thirst and vasopressin secretion present clinically in one of three ways: as hypotonic polyuria (DI), as hypodipsic hyponatremia, and as hyponatremia. In evaluating a patient with DI, the major challenge is to differentiate between primary polydipsia and neurogenic and nephrogenic DI. This is best accomplished through a series of steps that start with simple clinical observation, and progress, as necessary, to more complicated diagnostic procedures (Fig. 1). If the diagnosis is not clear from the clinical setting and the patient's history, the first step is to measure plasma osmolality and sodium under conditions of ad libitum fluid intake. If the results are clearly above the upper limit of normal range, primary polydipsia is excluded and the work-up can proceed directly to administration of vasopressin or DDAVP and/or a measurement of plasma vasopressin levels to differentiate between neurogenic and nephrogenic DI. If basal plasma osmolality and sodium fall within normal range, the standard dehydration test should be performed. If urine osmolality does not increase above that of plasma despite evident dehydration, primary polydipsia is excluded and the effect of vasopressin or DDAVP on urine osmolality should be examined to differentiate between neurogenic and nephrogenic DI. If administration of antidiuretic hormone increases urine osmolality by more than 50 per cent, the patient has severe neurogenic DI. If the increase in urine osmolality is less than 50 per cent, the patient has nephrogenic DI. In patients who do not concentrate urine above that of plasma in response to dehydration, the best approach is to measure plasma vasopressin, osmolality, and sodium after the latter have been increased above normal range by dehydration and/or infusion of hypertonic saline. When these results are plotted on a suitable nomogram (Fig. 2), neurogenic DI can be clearly diagnosed from the relative deficiency of vasopressin. In patients with normal vasopressin levels, primary polydipsia can be differentiated from nephrogenic DI by examining the relationship of urine osmolality to plasma vasopressin (Fig. 3), obtained during dehydration and/or graded vasopressin infusion. In evaluating a patient with sustained hypernatremia, it is only necessary to assess thirst, which can be done by a simple bedside observation. In a patient without obvious neurologic or cognitive impairment, absence of thirst in the face of plasma osmolality above 305 mosm/kg (plasma s

Topics: Humans; Thirst; Vasopressins; Water-Electrolyte Imbalance

Topics: Animals; Humans; Thirst; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Topics: Adult; Aged; Female; Humans; Hyponatremia; Male; Middle Aged; Pneumonia; Vasopressins; Water-Electrolyte Imbalance

Topics: Animals; Humans; Thirst; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

It is apparent that renal water retention in patients with advanced liver disease constitutes a fascinating clinical constellation with numerous and diverse causes and an elusive pathophysiology. The dissociation between elevated AVP levels and the attendant changes in renal water handling under diverse experimental conditions, and the demonstration of an impairment in renal water excretion in response to prostaglandin synthetase inhibition, underscore the multifactorial nature of the derangement. It is likely that the development of impaired renal water handling is attributable to a panoply of several hormonal or neural mediators, or both, acting in concert. Additional insight into this fascinating problem must await further characterization of some of the mediators and a delineation of their pathophysiologic role.

Topics: Body Water; Catecholamines; Glomerular Filtration Rate; Humans; Hyponatremia; Kidney; Liver Cirrhosis; Liver Diseases; Prostaglandins; Sympathetic Nervous System; Vasopressins; Water-Electrolyte Imbalance

Topics: Adrenergic beta-Antagonists; Anemia, Hemolytic; Animals; Antihypertensive Agents; Cyclic AMP; Factor XII; Humans; Hydralazine; Hypertension, Malignant; Labetalol; Platelet Aggregation; Prostaglandins F; Rabbits; Rats; Renin-Angiotensin System; Thromboplastin; Vasopressins; Water-Electrolyte Imbalance

Topics: Animals; Blood; Blood Pressure; Blood Volume; Diabetes Insipidus; Diuresis; Female; Humans; Hyperaldosteronism; Hypernatremia; Hyponatremia; Hypothalamus; Lung Neoplasms; Nausea; Osmolar Concentration; Pituitary Gland, Posterior; Pregnancy; Pressoreceptors; Sodium; Thirst; Urine; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Topics: Addison Disease; Aldosterone; Endocrine Glands; Glomerular Filtration Rate; Humans; Hydrocortisone; Inappropriate ADH Syndrome; Kidney; Parathyroid Hormone; Thyroid Hormones; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance; Wounds and Injuries

Topics: Animals; Central Nervous System Diseases; Diagnosis, Differential; Humans; Hyponatremia; Hypothalamo-Hypophyseal System; Inappropriate ADH Syndrome; Neoplasms; Nephrons; Vasopressins; Water-Electrolyte Imbalance

The total restoration of urinary concentrating ability of the DI rat given daily injections of vasopressin takes several weeks, although complete osmotic equilibrium across the collecting duct is manifest within hours. This suggests that there may be other deficiencies of the renal concentrating mechanism that, if corrected by vasopressin treatment, are corrected more slowly. I have focussed on just three possibilities. First, the morphology of the medullary interstitium is different from normal rats. Perhaps associated with this finding are alterations in the levels of medullary glycosaminoglycans which may have a role to play in water balance. Functional and morphological changes in the juxtamedullary nephrons are also evident. Second, the possibility exists that the countercurrent multiplier of the DI rat operates less efficiently than in the normal animal. Finally, reduced synthesis of PGs in the renal medulla of DI rats may also influence the concentrating mechanism, although in a favorable direction. While most (if not all) of these differences are secondary to the lack of vasopressin, in some instances it appears that it is the high water turnover (possibly the altered chemical composition of the medullary interstitium) that is the primary culprit. While the DI rat remains an excellent model for the study of water balance and the action of vasopressin, the presence of multiple defects within the system should be borne in mind. This is particularly true when comparing data obtained following acute treatment with vasopressin versus that following chronic treatment.

Topics: Adenylyl Cyclases; Animals; Arginine Vasopressin; Deamino Arginine Vasopressin; Diabetes Insipidus; Disease Models, Animal; Glomerular Filtration Rate; Glycosaminoglycans; Kidney; Kidney Concentrating Ability; Kidney Medulla; Loop of Henle; Nephrons; Osmolar Concentration; Prostaglandins; Rats; Rats, Brattleboro; Rats, Mutant Strains; Vasopressins; Water-Electrolyte Imbalance

The osmolality of body fluids is normally maintained within a narrow range. This constancy is achieved largely via hypothalamic osmo-receptors that regulate thirst and arginine vasopressin, the antidiuretic hormone (ADH). Anything that interferes with the full expression of either osmoregulatory function exposes the patient to the hazards of abnormal increases or decreases in plasma osmolality. Hyposmolality is almost always due to a defect in water excretion. Increased intake may contribute to the problem but is rarely, if ever, a sufficient cause. Impaired water excretion can be due to a primary defect in the osmoregulation of ADH (inappropriate antidiuresis) or secondary to nonosmotic stimuli like hypovolemia or nausea. The two types differ in clinical presentation and treatment. Resetting of the ADH osmostat is commonly associated with resetting of the thirst osmostat. Hyperosmolarity is almost always due to deficient water intake. Excessive excretion may contribute to the problem but is never a sufficient cause. Impaired water intake can result from a defect in either the osmoregulation of thirst of the necessary motor responses. Thirst may be deficient because of primary osmoreceptor damage as in the syndrome of adipsic hypernatremia or secondary to nonosmotic influences on the set of the system. They are distinguishable by the clinical presentation as well as the type of ADH defects with which they are associated. So-called essential hypernatremia due to primary resetting of the osmostat has been postulated, but unambiguous evidence for such an entity has not yet been reported.

Topics: Body Water; Hemodynamics; Humans; Inappropriate ADH Syndrome; Osmolar Concentration; Sodium; Thirst; Vasopressins; Water-Electrolyte Imbalance

The evidence that prolactin is a fluid and electrolyte regulator in mammals is reviewed, with particular emphasis on the renal actions of prolactin. Prolactin receptors are found in mammalian kidneys. Prolactin modulates renal formation of cyclic AMP and polyamines and it leads to demonstrable histological changes in the proximal tubules. The renal actions of prolactin primarily involve modulation of the effects of other hormones and are therefore critically dependent on the background physiological situation. Prolactin seems able to cause a prolonged reduction in water, sodium, and potassium excretion, a pattern that is imitated by no other hormone with the possible exception of growth hormone. Prolactin preparations can cause an acute antidiuresis, which may in part be related to contamination of prolactin preparations with vasopressin. However, most of the described effects cannot be explained by vasopressin contamination. This is particularly so with the effects of prolactin on water movements across fetal skin, the amniotic membrane, and in the eye where prolactin and vasopressin have diametrically opposite effects. It is concluded that prolactin is a regulator of fluid and electrolyte metabolism in mammals but that it is a modulator rather than a primary controlling factor.

Topics: Aldosterone; Animals; Drug Interactions; Glucocorticoids; Humans; Kidney; Prolactin; Receptors, Cell Surface; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Topics: Animals; Arginine Vasopressin; Chlorpropamide; Deamino Arginine Vasopressin; Diabetes Insipidus; Humans; Inappropriate ADH Syndrome; Lypressin; Vasopressins; Water-Electrolyte Imbalance

Topics: Humans; Osmolar Concentration; Syndrome; Vasopressins; Water-Electrolyte Imbalance

Topics: ACTH Syndrome, Ectopic; Humans; Lung Neoplasms; Nephrotic Syndrome; Paraneoplastic Syndromes; Renin; Vasopressins; Water-Electrolyte Imbalance

Topics: Adrenocorticotropic Hormone; Aldosterone; Blood Volume; Edema; Extracellular Space; Female; Glomerulonephritis; Humans; Hyaluronoglucosaminidase; Kidney; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Sodium; Vasopressins; Water-Electrolyte Imbalance

Topics: Brain Diseases; Diabetes Insipidus; Electrolytes; Humans; Hypernatremia; Hyponatremia; Postoperative Complications; Vasopressins; Water; Water Intoxication; Water-Electrolyte Imbalance

Topics: Adrenocorticotropic Hormone; Animals; Benzothiadiazines; Chlorpropamide; Corticotropin-Releasing Hormone; Diabetes Insipidus; Disease Models, Animal; Diuresis; Diuretics; Female; Hypothalamus; Male; Pituitary Gland, Anterior; Rats; Sodium Chloride Symporter Inhibitors; Thyroid Gland; Vasopressins; Water-Electrolyte Imbalance

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

Topics: Angiotensin II; Animals; Blood Pressure; Hypertension, Malignant; Hypertension, Renal; Hyponatremia; Juxtaglomerular Apparatus; Osmolar Concentration; Pepstatins; Plasma Volume; Rats; Renin; Saralasin; Vasopressins; Water-Electrolyte Imbalance

SIADH consists of hyponatremia and hyposmolality, continued urinary loss of sodium, excretion of an inappropriately concentrated urine, and absence of dehydration, usually in the presence of normal renal and adrenal function. The retention of excess water caused by the inappropriate secretion of antidiuretic hormone is central to the development of the syndrome. In pediatrics, SIADH is most commonly seen in patients with meningitis or postoperatively. Fluid restriction is vital in such patients to prevent the development of symptomatic SIADH. Fluid restriction alone will also result in the correction of serum electrolyte composition in patients with SIADH. Hypertonic saline should be used only in severely symptomatic patients.

Topics: Adult; Aldosterone; Blood Volume; Child; Diuresis; Drinking; Ethanol; Humans; Hyponatremia; Kidney Concentrating Ability; Kidney Tubules, Distal; Kidney Tubules, Proximal; Lithium; Osmolar Concentration; Saline Solution, Hypertonic; Sodium; Syndrome; Vasopressins; Water Intoxication; Water-Electrolyte Imbalance

Topics: Acidosis, Renal Tubular; Aldosterone; Ascites; Diuretics; Hepatic Encephalopathy; Humans; Hypokalemia; Kidney Failure, Chronic; Kidney Transplantation; Kidney Tubules, Distal; Liver Cirrhosis; Liver Transplantation; Sodium; Transplantation, Homologous; Uremia; Vasopressins; Water-Electrolyte Imbalance

Copeptin, the C-terminal moiety of provasopressin, is cosecreted with vasopressin. Copeptin may be a useful parameter to characterize disorders of water homeostasis and can be readily measured in plasma or serum. However, it is unknown to date how circulating copeptin and vasopressin levels correlate at different plasma osmolalites.. To correlate plasma copeptin with plasma osmolality and vasopressin concentrations in healthy subjects during iso-, hypo-, and hyperosmolar states.. Plasma osmolalities, copeptin, and vasopressin levels were measured in 20 volunteers at baseline, after an oral water load, and during and after iv infusion of 3% saline. Correlation coefficients were determined between plasma osmolalites and copeptin and vasopressin concentrations, as well as between vasopressin and copeptin concentrations.. Median plasma osmolalities decreased from 290 mOsm/kg (range, 284-302) at baseline to 281 (273-288) mOsm/kg after water load and rose to 301 (298-307) mOsm/kg after hypertonic saline. Median plasma copeptin concentrations decreased from 3.3 (1.1-36.4) pm at baseline to 2.0 (0.9-10.4) pm after water load and increased to 13.6 (3.7-43.3) pm after hypertonic saline. Vasopressin and copeptin concentrations correlated with plasma osmolality (Spearman's rank correlation coefficient 0.49 and 0.77, respectively). There was a close correlation of vasopressin and copeptin concentrations (Spearman's rank correlation coefficient 0.8).. Plasma vasopressin and copeptin correlate strongly over a wide range of osmolalities in healthy individuals. Therefore, the measurement of copeptin, which remains stable for several days, is a useful alternative to vasopressin measurements and will likely facilitate the differential diagnosis of disorders of water metabolism.

Topics: Adult; Female; Glycopeptides; Health Status; Humans; Hypotonic Solutions; Male; Osmolar Concentration; Saline Solution, Hypertonic; Vasopressins; Water; Water-Electrolyte Balance; Water-Electrolyte Imbalance; Young Adult

Noradrenergic A2 neurons of the nucleus of the solitary tract (NTS) have been suggested to contribute to body fluid homeostasis and cardiovascular regulation. In the present study, we investigated the effects of lesions of A2 neurons of the commissural NTS (cNTS) on the c-Fos expression in neurons of the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei, arterial pressure, water intake, and urinary excretion in rats with plasma hyperosmolality produced by intragastric 2 M NaCl (2 ml/rat). Male Holtzman rats (280-320 g) received an injection of anti-dopamine-β-hydroxylase-saporin (12.6 ng/60 nl; cNTS/A2-lesion, n = 28) or immunoglobulin G (IgG)-saporin (12.6 ng/60 nl; sham, n = 24) into the cNTS. The cNTS/A2 lesions increased the number of neurons expressing c-Fos in the magnocellular PVN in rats treated with hypertonic NaCl (90 ± 13, vs. sham: 47 ± 20; n = 4), without changing the number of neurons expressing c-Fos in the parvocellular PVN or in the SON. Contrary to sham rats, intragastric 2 M NaCl also increased arterial pressure in cNTS/A2-lesioned rats (16 ± 3, vs. sham: 2 ± 2 mmHg 60 min after the intragastric load; n = 9), an effect blocked by the pretreatment with the vasopressin antagonist Manning compound (0 ± 3 mmHg; n = 10). In addition, cNTS/A2 lesions enhanced hyperosmolality-induced water intake (10.5 ± 1.4, vs. sham: 7.7 ± 0.8 ml/60 min; n = 8-10), without changing renal responses to hyperosmolality. The results suggest that inhibitory mechanisms dependent on cNTS/A2 neurons reduce water intake and vasopressin-dependent pressor response to an acute increase in plasma osmolality.

Topics: Adrenergic Neurons; Animals; Appetite Regulation; Blood Pressure; Body Water; Male; Neurovascular Coupling; Osmolar Concentration; Osmoregulation; Rats; Rats, Sprague-Dawley; Solitary Nucleus; Vasoconstriction; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Because of antidiuretic hormone (ADH) disorder on production or function we can observe dysnatremia. In the absence of production by posterior pituitary, central diabetes insipidus (DI) occurs with hypernatremia. There are hereditary autosomal dominant, autosomal recessive or X- linked forms. When ADH is secreted but there is an alteration on his receptor AVPR2, it is a nephrogenic diabetes insipidus in acquired or hereditary form. We can make difference on AVP levels and/or on desmopressine response which is negative in nephrogenic forms. Hyponatremia occurs when there is an excess of ADH production: it is a euvolemic hypoosmolar hyponatremia. The most frequent etiology is SIADH (syndrome of inappropriate secretion of ADH), a diagnostic of exclusion which is made after eliminating corticotropin deficiency and hypothyroidism. In case of brain injury the differential diagnosis of cerebral salt wasting (CSW) syndrome has to be discussed, because its treatment is perfusion of isotonic saline whereas in SIADH, the treatment consists in administration of hypertonic saline if hyponatremia is acute and/or severe. If not, fluid restriction demeclocycline or vaptans (antagonists of V2 receptors) can be used in some European countries. Four types of SIADH exist; 10 % of cases represent not SIADH but SIAD (syndrome of inappropriate antidiuresis) due to a constitutive activation of vasopressin receptor that produces water excess. c 2013 Published by Elsevier Masson SAS.

Topics: Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diagnosis, Differential; Humans; Hypernatremia; Hyponatremia; Inappropriate ADH Syndrome; Pituitary Diseases; Pituitary Gland, Posterior; Receptors, Vasopressin; Sodium Chloride; Vasopressins; Water-Electrolyte Imbalance

Arginine vasopressin (AVP) affects kidney function via vasopressin V2 receptors that are linked to activation of adenylyl cyclase (AC) and an increase in cyclic adenosine monophosphate formation. AVP/cyclic adenosine monophosphate enhance the phosphorylation of the Na-K-2Cl cotransporter (NKCC2) at serine residue 126 (pS126 NKCC2) and of the Na-Cl cotransporter (NCC) at threonine 58 (pT58 NCC). The isoform(s) of AC involved in these responses, however, were unknown. Phosphorylation of S126 NKCC2 and T58 NCC, induced by the V2 receptor agonist (1-desamino-8-D-arginine vasopressin) in wild-type mice, is lacking in knockout mice for AC isoform 6 (AC6). With regard to NKCC2 phosphorylation, the stimulatory effect of 1-desamino-8-D-AVP and the defect in AC6(-/-) mice seem to be restricted to the medullary portion of the thick ascending limb. AC6 is also a stimulator of total renal NKCC2 protein abundance in medullary and cortical thick ascending limb. Consequently, mice lacking AC6 have lower NKCC2 expression and a mild Bartter syndrome-like phenotype, including lower plasma concentrations of K+ and H+ and compensatory upregulation of NCC. Increased AC6-independent phosphorylation of NKCC2 at S126 might help to stabilize NKCC2 activity in the absence of AC6. Renal AC6 determines total NKCC2 expression and mediates vasopressin-induced NKCC2/NCC phosphorylation. These regulatory mechanisms, which are defective in AC knockout mice, are likely responsible for the observed mild Bartter syndrome.

Topics: Adenylyl Cyclases; Animals; Antidiuretic Agents; Bartter Syndrome; Deamino Arginine Vasopressin; Female; Gene Expression Regulation; Kidney; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Microscopy, Confocal; Phosphorylation; Sodium Chloride Symporters; Sodium-Potassium-Chloride Symporters; Solute Carrier Family 12, Member 1; Vasopressins; Water-Electrolyte Imbalance

The nucleus of the solitary tract (NTS) is the primary site of visceral afferents to the central nervous system. In the present study, we investigated the effects of lesions in the commissural portion of the NTS (commNTS) on the activity of vasopressinergic neurons in the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei, plasma vasopressin, arterial pressure, water intake, and sodium excretion in rats with plasma hyperosmolality produced by intragastric 2 M NaCl (2 ml/rat). Male Holtzman rats with 15-20 days of sham or electrolytic lesion (1 mA; 10 s) of the commNTS were used. CommNTS lesions enhanced a 2 M NaCl intragastrically induced increase in the number of vasopressinergic neurons expressing c-Fos in the PVN (28 ± 1, vs. sham: 22 ± 2 c-Fos/AVP cells) and SON (26 ± 4, vs. sham: 11 ± 1 c-Fos/AVP cells), plasma vasopressin levels (21 ± 8, vs. sham: 6.6 ± 1.3 pg/ml), pressor responses (25 ± 7 mmHg, vs. sham: 7 ± 2 mmHg), water intake (17.5 ± 0.8, vs. sham: 11.2 ± 1.8 ml/2 h), and natriuresis (4.9 ± 0.8, vs. sham: 1.4 ± 0.3 meq/1 h). The pretreatment with vasopressin antagonist abolished the pressor response to intragastric 2 M NaCl in commNTS-lesioned rats (8 ± 2.4 mmHg at 10 min), suggesting that this response is dependent on vasopressin secretion. The results suggest that inhibitory mechanisms dependent on commNTS act to limit or counterbalance behavioral, hormonal, cardiovascular, and renal responses to an acute increase in plasma osmolality.

Topics: Animals; Blood Pressure; Drinking; Kidney; Male; Osmolar Concentration; Oxytocin; Paraventricular Hypothalamic Nucleus; Proto-Oncogene Proteins c-fos; Rats; Rats, Sprague-Dawley; Solitary Nucleus; Supraoptic Nucleus; Vasopressins; Water-Electrolyte Imbalance

Topics: Adult; Blood Gas Analysis; Diabetes Insipidus; Female; Fluid Therapy; Humans; Osmolar Concentration; Perioperative Care; Pituitary Gland; Pituitary Neoplasms; Polyuria; Postoperative Complications; Sodium; Vasopressins; Water-Electrolyte Imbalance

The expression of the novel peptide apelin and its receptor APJ within specific regions of the brain, in particular the magnocellular neurones of the hypothalamus and the circumventricular organs, has implicated the apelinergic system in mechanisms controlling fluid homeostasis. In addition, apelin and APJ are considered to be involved in controlling arginine vasopressin (AVP) secretion into the circulation and release within the hypothalamic-neurohypophysial system. To clarify the role of APJ during regulation of fluid homeostasis, we compared the effects of osmotic stimulation on the urinary concentrating capacities and central nervous system responses of salt-loaded (SL) and water-deprived (WD) female APJ knockout (APJ(-/-)) mice and wild-type controls. SL resulted in a significantly increased urine volume in APJ(-/-) mice compared to wild-type controls, whereas WD in APJ(-/-) mice failed to reduce urine volume as seen in wild-type controls. AVP transcripts in the supraoptic and paraventricular nuclei and plasma AVP concentrations were significantly attenuated in SL APJ(-/-) mice compared to SL wild-type, but increased comparably in wild-type and APJ(-/-) mice after WD. Analysis of c-fos mRNA expression in the median preoptic nucleus and subfornical organ in response to either WD or SL showed attenuated expression in APJ(-/-) compared to wild-type mice. These findings further implicate the apelinergic system in mechanisms controlling fluid homeostasis, particularly at a neuroendocrine level, and suggest stimulus-specific involvement in vasopressinergic activity.

Topics: Animals; Apelin Receptors; Body Fluids; Female; Gene Expression Regulation; Homeostasis; Mice; Mice, Inbred C57BL; Mice, Knockout; Neurosecretory Systems; Osmotic Pressure; Physical Stimulation; Receptors, G-Protein-Coupled; Salts; Stress, Physiological; Vasopressins; Water Deprivation; Water-Electrolyte Imbalance

Water retention in advanced cirrhosis and ascites may involve disturbances in renal distal tubular function and in the vasopressin system.. Twelve patients with Child B cirrhosis and ascites were compared with 11 patients with Child C cirrhosis and ascites. The subjects were studied during a 400 ml/h oral water load.. Child C patients had a lower baseline glomerular filtration rate (32 vs 63 ml/min, P<0.001) and a lower urinary flow rate (V(u)) (0.86 vs 1.95 ml/min, P<0.001) than the Child B patients. However, the free water clearance (C(H2O)) did not differ (-0.60 vs -0.21 ml/min, P=0.20). After the water loading, plasma vasopressin (AVP) decreased significantly in both the groups (P<0.05). The Child B patients had increased V(u) (1.95-3.24 ml/min, P<0.001) and C(H2O) (-0.21-1.21 ml/min, P<0.01) and distal fractional water excretion (10.5 vs 0% in Child C, P=0.01) and aquaporin-2 (AQP2) (P<0.058) after water loading. In contrast, the Child C patients did not have increased V(u) and C(H2O) in response to the water and the decrease in AVP. Furthermore, the markers of distal tubular water regulation, AQP2 excretion and distal fractional water excretion, were unaltered.. In Child C cirrhosis, ascites and mild hyponatraemia, there is an impaired ability to excrete solute-free water. The patients are characterised by a low glomerular filtration rate, a low distal tubular flow and an inability to increase free water clearance during water loading. This may be related to a vasopressin-independent production of AQP2.

Topics: Ascites; Body Water; Diuresis; Female; Humans; Kidney Tubules, Distal; Liver Cirrhosis; Male; Middle Aged; Severity of Illness Index; Vasopressins; Water-Electrolyte Imbalance

Topics: Humans; Radioimmunoassay; Vasopressins; Water-Electrolyte Imbalance

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

Increased extracellular fluid volume (ECF) characterizes compensated cirrhosis. To identify the mechanisms of fluid retention in cirrhosis through clearance methods, 10 control and 10 preascitic rats with CCl(4)-induced cirrhosis were studied following i.v. loading with 1 ml 5% glucose solution. Glomerular filtration rate and renal plasma flow were evaluated through inulin and para-aminohippurate clearances; water and electrolyte handling was assessed measuring urine and plasma osmolarity, electrolyte excretions, and tubular solute-free water reabsorption (TFWR = osmolar clearance minus urinary output); ECF was assessed through hormonal status determination. After water loading, cirrhotic rats had increased ECF (lower plasma renin activity and aldosterone and higher atrial natriuretic peptide levels, all P<0.03), solute-free water retention (increased TFWR and decreased plasma osmolarity, all P<0.05), reduced absolute and fractional sodium excretions (P<0.05). Cirrhotic rats showed sodium retention in the medullary thick ascending limb of Henle's loop (i.e. increased values of TFWR for any given value of osmolar clearance). Trans-tubular potassium gradient in medullary collecting duct was similar in the two groups (P=0.55), ruling out aldosterone-dependent sodium retention and potassium hyper-secretion. In experimental preascitic cirrhosis NaCl retention in the ascending limb of Henle's loop increases medullary interstitial tonicity leading to vasopressin-independent water back-diffusion in thin descending limb of Henle's loop and collecting duct.

Topics: Aldosterone; Animals; Atrial Natriuretic Factor; Extracellular Fluid; Glomerular Filtration Rate; Kidney; Kidney Tubules, Distal; Liver Cirrhosis; Loop of Henle; Male; Osmolar Concentration; Potassium; Rats; Rats, Wistar; Renin; Sodium; Vasopressins; Water; Water-Electrolyte Imbalance

Schizophrenia, many believe, reflects an enhanced vulnerability to psychological stress. Controlled exposure to stressors, however, has produced inconclusive results, particularly with regards to neurohormones. Some of the variability may be attributable to the nature and psychological significance of the stimulus and failure to control physiologic confounds. In addition, it is possible that the heterogeneity of schizophrenia is an important factor. In a carefully designed study and in a controlled setting, we measured the neuroendocrine response of eight polydipsic hyponatremic (PHS), seven polydipsic normonatremic (PNS), and nine nonpolydipsic normonatremic (NNS) (ie normal water balance) schizophrenic in-patients as well as 12 healthy controls (HC) to two different stressors: one of which appears to influence neuroendocrine secretion through its psychological (cold pressor) and the other (upright posture) through its systemic actions. Subjects in the three psychiatric groups were stabilized and acclimated to the research setting, and all received saline to normalize plasma osmolality. Following the cold pressor, plasma adrenocorticotropin and cortisol levels showed a more prolonged rise in PHS patients relative to PNS patients. NNS patients, in contrast, exhibited blunted responses relative to both of the polydipsic groups and the HC. Peak vasopressin responses were also greater in PHS and blunted in NNS patients. Responses to the postural stimulus were similar across patient groups. These findings provide a mechanism for life threatening water intoxication in schizophrenia; help to reconcile conflicting findings of stress responsiveness in schizophrenia; and potentially identify a discrete patient subset with enhanced vulnerability to psychological stress.

Topics: Adult; Cold Temperature; Drinking; Endocrine System Diseases; Female; Humans; Hyponatremia; Hypothalamo-Hypophyseal System; Male; Middle Aged; Neurosecretory Systems; Schizophrenia; Stress, Psychological; Thirst; Vasopressins; Water Intoxication; Water-Electrolyte Imbalance

Topics: Fluid Therapy; Humans; Hyponatremia; Interleukin-6; Physical Endurance; Vasopressins; Water-Electrolyte Imbalance

Topics: Animals; Dogs; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins; Water-Electrolyte Imbalance

Vasopressin is a critical regulator of water homeostasis. There are two major receptors for vasopressin: V1 and V2 receptors. Disturbances in water balance are commonly encountered in clinical practice and can be divided into disorders of urinary dilution and concentration. The major representatives of such disorders are diabetes insipidus and the syndrome of inappropriate secretion of antidiuretic hormone (SI ADH). Recent studies show that genetic forms of nephrogenic diabetes insipidus are due to mutations in the genes coding for the vasopressin V2 receptor (V2R) or aquaporin-2 (AQP2). Identification of the genes involved and analysis of the cellular fate of the V2R and AQP2 mutants are relevant for understanding the functioning of the V2R and AQP2 protein. These developments also have implications for future therapeutic options. The development of nonpeptide vasopressin receptor antagonists (VRAs) offers prospects for the treatment of euvolaemic (SI ADH) or hypervolaemic hyponatraemia (congestive heart failure or cirrhosis). Several nonpeptide VRAs are now in various stages of clinical trials. At present, only conivaptan is registered by the FD A for intravenous treatment of euvolaemic and hypervolaemic hyponatremia. A recent long-term study comparing tolvaptan with placebo in patients with chronic heart failure showed no reduction in risk of death and hospitalisation.

Topics: Antidiuretic Hormone Receptor Antagonists; Diabetes Insipidus, Nephrogenic; Humans; Inappropriate ADH Syndrome; Mutation; Receptors, Vasopressin; Vasopressins; Water; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Disorders of water and sodium balance are frequently seen in patients with severe brain injury (SBI), and may worsen their prognosis.. To evaluate vasopressin (AVP) serum levels and sodium and water balance disorders during the first week post-injury in patients with SBI.. Thirty-six adult patients with SBI (admission Glasgow Coma Scale score < or= 8) and an estimated time of injury

Topics: Acute Disease; Adult; Biomarkers; Brain Injuries; Case-Control Studies; Female; Glasgow Coma Scale; Humans; Male; Osmolar Concentration; Prospective Studies; Sodium; Vasopressins; Water-Electrolyte Imbalance

The present study sought to determine whether chemical destruction of peripheral catecholaminergic fibers with 6-hydroxydopamine (6OHDA) attenuates vasopressin (VP) and oxytocin (OT) secretion stimulated by hemorrhage, hypotension, and hyperosmolality. Rats received 6OHDA (100 mg/kg iv) or vehicle (1 ml/kg iv) on days 1 and 7, and experiments were performed on day 8. Serial hemorrhage (4 samples of 2 ml per 300 g body wt at 10-min intervals) increased plasma VP and OT levels in both groups; however, the increase in plasma VP and OT levels was significantly attenuated in 6OHDA-treated vs. control rats despite a significantly lower mean arterial blood pressure. Similarly, the increase in plasma VP and OT levels in response to hypotension produced by the selective arteriolar vasodilator diazoxide was significantly attenuated in 6OHDA-treated rats. In marked contrast to hemorrhage and hypotension, hyperosmolality produced by an infusion of 1 M NaCl (2 ml/h iv) stimulated increases in plasma VP and OT levels that were not different between 6OHDA-treated and control rats. In a parallel set of experiments, intravenous 6OHDA treatment reduced dopamine--hydroxylase immunoreactivity in the posterior pituitary but had no substantial effect in the hypothalamic paraventricular and supraoptic nuclei. In each experiment, the pressor response to tyramine (250 microg/kg iv) was significantly attenuated in 6OHDA-treated rats, thereby confirming that 6OHDA treatment destroyed sympathetic catecholaminergic fibers. Collectively, these findings suggest that catecholaminergic fibers located outside the blood-brain barrier contribute to VP and OT secretion during hemorrhage and arterial hypotension.

Topics: Animals; Diazoxide; Dopamine beta-Hydroxylase; Hemorrhage; Hypotension; Hypothalamus; Injections, Intravenous; Male; Oxidopamine; Oxytocin; Pituitary Gland, Posterior; Rats; Rats, Sprague-Dawley; Sympatholytics; Tyramine; Vasopressins; Water-Electrolyte Imbalance

Topics: Abdomen, Acute; Adult; Aged; Hemostatics; Humans; Liver Diseases; Male; Middle Aged; Multiple Trauma; Pancreatic Neoplasms; Pancreaticoduodenectomy; Rupture, Spontaneous; Vasopressins; Water-Electrolyte Imbalance

To examine whether children with univentricular defects have intrinsic dysfunction in the natriuretic peptide system.. We compared plasma levels of the fluid-regulating hormone vasopressin (antidiuretic hormone), aldosterone, atrial natriuretic peptide, and brain natriuretic peptide in children with congenital univentricular and biventricular defects. We enrolled 27 patients with univentricular defects and 27 patients with biventricular cardiac defects. Children who underwent Fontan and Glenn procedures were considered as patients with univentricular cardiac defects; children who underwent repair of tetralogy of Fallot or subaortic stenosis were considered as controls with biventricular defects.. Preoperative plasma atrial natriuretic peptide, brain natriuretic peptide, antidiuretic hormone, and aldosterone were comparable in both groups. Although plasma cyclic guanosine monophosphate levels were comparable between groups, there was a significant correlation between molar concentrations of plasma cyclic guanosine monophosphate and plasma atrial natriuretic peptide ( r = 0.42) and brain natriuretic peptide ( r = 0.44) in the biventricular group, but not in the univentricular group ( r = 0.19 for atrial natriuretic peptide; r = 0.13 for brain natriuretic peptide). All patients had a significant postoperative increase in plasma antidiuretic hormone. A significant postoperative increase in plasma brain natriuretic peptide was found in the patients with biventricular, but not univentricular, defects. In contrast, a significant increase in plasma aldosterone was observed only in the patients with univentricular defects.. There were distinct differences between univentricular and biventricular groups in their perioperative plasma fluid-regulating hormone responses. Specifically, patients with univentricular defects may have abnormal natriuretic peptide secretion and function. The natriuretic dysfunction may be on the basis of hypoplastic ventricular development.

Topics: Age Factors; Aldosterone; Analysis of Variance; Atrial Natriuretic Factor; Biomarkers; Cardiopulmonary Bypass; Case-Control Studies; Child, Preschool; Cyclic GMP; Down-Regulation; Female; Fontan Procedure; Heart Ventricles; Humans; Infant; Male; Mineralocorticoid Receptor Antagonists; Natriuretic Peptide, Brain; Risk Factors; Second Messenger Systems; Signal Transduction; Time Factors; Up-Regulation; Vasopressins; Water-Electrolyte Imbalance

The present study sought to determine whether an acute increase in arterial blood pressure (ABP) reduces plasma vasopressin (VP) levels stimulated by ANG II or hyperosmolality. During an intravenous infusion of ANG II (100 ng.kg(-1).min(-1)), attenuation of the ANG II-evoked increase in ABP with diazoxide or minoxidil did not further enhance plasma VP levels in rats. When VP secretion was stimulated by an infusion of hypertonic saline, coinfusion of the alpha-adrenergic agonist phenylephrine (PE) significantly increased ABP but did not reduce plasma VP levels. In fact, plasma VP levels were enhanced. The enhancement of plasma VP levels cannot be explained by a direct stimulatory action of PE, as plasma VP levels of isosmotic rats did not change during a similar infusion of PE. An infusion of endothelin-1 in hyperosmotic rats significantly raised ABP but did not reduce plasma VP levels; rather, VP levels increased as observed with PE. In alpha-chloralose-anesthetized rats infused with hypertonic saline, inflation of an aortic cuff to increase ABP and stimulate arterial baroreceptors did not reduce plasma VP levels. In each experiment, plasma oxytocin levels paralleled plasma VP levels. Collectively, the present findings suggest that an acute increase in ABP does not inhibit VP secretion.

Topics: Angiotensin II; Animals; Blood Pressure; Electrophysiology; Endothelins; Injections, Intravenous; Male; Neurons; Osmolar Concentration; Oxytocin; Phenylephrine; Rats; Rats, Sprague-Dawley; Renin; Saline Solution, Hypertonic; Stimulation, Chemical; Vasoconstrictor Agents; Vasopressins; Water-Electrolyte Imbalance

Measurement of plasma osmolality (Posm) and plasma vasopressin (VP) concentration in response to hypertonicity is regarded as the gold standard for the assessment of VP release in polyuric conditions. Yet the interpretation of the VP curve as a function of Posm may be hampered by the occurrence of VP pulses. To determine whether VP is secreted in a pulsatile fashion in the dog and whether stimulation of VP release changes the secretion pattern of VP, we measured VP at 2-min intervals for 2 h under basal conditions, after 12 h of water deprivation, and during osmotic stimulation with hypertonic saline (20%) in eight healthy dogs. Vasopressin was secreted in a pulsatile fashion with a wide variation in number of VP pulses, VP pulse duration, and VP pulse amplitude and height. After water deprivation, total and basal VP secretion, the number of significant VP pulses, as well as the pulse characteristics did not differ from the basal situation. During osmotic stimulation, there was a large increase in both basal and pulsatile VP secretion, and the number of VP pulses and VP pulse height and amplitude were significantly increased. The VP pulse amplitude correlated significantly with the basal plasma VP concentration during osmotic stimulation. It is concluded that VP is secreted in a pulsatile manner in healthy dogs. The basal and pulsatile VP secretion increases during osmoreceptor-mediated stimulation. The VP pulses may occur to the magnitude that they may be interpreted as erratic bursts, when occurring in the hypertonic saline infusion test.

Topics: Analysis of Variance; Animals; Area Under Curve; Dogs; Female; Osmolar Concentration; Periodicity; Reference Values; Saline Solution, Hypertonic; Vasopressins; Water Deprivation; Water-Electrolyte Balance; Water-Electrolyte Imbalance

The vasopressin (VP) magnocellular neurosecretory cells (MNCs) in the supraoptic and paraventricular (PVN) nuclei are regulated by estrogen and exhibit robust expression of estrogen receptor (ER)-beta. In contrast, only approximately 7.5% of oxytocin (OT) MNCs express ER-beta. We examined the osmotic regulation of ER-beta mRNA expression in MNCs using quantitative in situ hybridization histochemistry. Hyper-osmolality induced via 2% hypertonic saline ingestion significantly decreased, whereas sustained hypo-osmolality induced via d-d-arginine VP and liquid diet increased ER-beta mRNA expression in MNCs (p < 0.05). Thus, the expression of ER-beta mRNA correlated inversely with changes in plasma osmolality. Because hyper-osmolality is a potent stimulus for VP and OT release, this suggests an inhibitory role for ER-beta in MNCs. Immunocytochemistry demonstrated that the decrease in ER-beta mRNA was translated into depletion of receptor protein content in hyper-osmotic animals. Numerous MNCs were positive for ER-beta in control animals, but they were virtually devoid of ER-beta-immunoreactivity (IR) in hyper-osmotic animals. The osmotically induced decrease in ER-beta expression was selective for MNCs because ER-beta-IR remained unaltered in PVN parvocellular neurons. Plasma estradiol and testosterone were not correlated with ER-beta mRNA expression after osmotic manipulation, suggesting that ER-beta expression was not driven by ligand availability. Expression of FOS-IR in MNCs with attenuated ER-beta-IR, and the absence of FOS-IR in parvocellular neurons that retain ER-beta-IR suggest a role for neuronal activation in the regulation of ER-beta expression in MNCs. Thus, osmotic modulation of ER-beta expression in MNCs may augment or attenuate an inhibitory effect of gonadal steroids on VP release.

Topics: Animals; Blood Volume; Body Weight; Estrogen Receptor beta; Hematocrit; Hormones; Hypernatremia; Hyponatremia; Male; Neurons; Osmolar Concentration; Osmotic Pressure; Oxytocin; Paraventricular Hypothalamic Nucleus; Rats; Rats, Sprague-Dawley; Receptors, Estrogen; Sodium Chloride; Supraoptic Nucleus; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

We present a case to illustrate the importance of emphasizing elementary physiology to deduce the basis for the acute onset of polyuria and hypernatremia. An imaginary consultation with Professor McCance is utilized to illustrate how a clinician-physiologist would have explained why these abnormalities developed and how they should have been treated. His approach began with a consideration of the most impressive abnormality. His analysis relied heavily on deductions and the anticipation of the expected responses to a stimulus in quantitative terms. The goals of therapy became evident after he performed mass balance calculations. Professor McCance would not understand why modern clinicians abandoned this form of analysis.

Topics: Adult; Female; Humans; Hypernatremia; Intracranial Aneurysm; Polyuria; Urination; Vasopressins; Water-Electrolyte Imbalance

The mechanisms underlying the prevention of age-related polyuria by chronic food restriction were investigated in female WAG/Rij rats. The decreased osmolality of renal papilla observed in senescent rats was not corrected by food restriction. A reduced urea content in the inner medulla of senescent rats, fed ad libitum or food-restricted, was suggested by the marked decrease in expression of UT-A1 and UT-B1 urea transporters. Aquaporin-2 (AQP2) downregulation in the inner medulla of senescent rats was partially prevented by food restriction. Both AQP2 and the phosphorylated form of AQP2 (p-AQP2), the presence of which was diffuse within the cytoplasm of collecting duct principal cells in normally fed senescent rats, were preferentially targeted at the apical region of the cells in food-restricted senescent animals. Plasma vasopressin (AVP) was similar in 10- and 30-mo-old rats fed ad libitum, but was doubled in food-restricted 30-mo-old rats. This study indicates that 1) kidney aging is associated with a marked decrease in AQP2, UT-A1, and UT-B1 expression in the inner medulla and a reduced papillary osmolality; and 2) the prevention of age-related polyuria by chronic food restriction occurs through an improved recruitment of AQP2 and p-AQP2 to the apical membrane in inner medulla principal cells, permitted by increased plasma AVP concentration.

Topics: Aging; Animals; Aquaporin 2; Aquaporin 6; Aquaporins; Carrier Proteins; Cell Polarity; Eating; Female; Kidney; Kidney Medulla; Kidney Tubules; Membrane Glycoproteins; Membrane Transport Proteins; Osmolar Concentration; Phosphorylation; Polyuria; Protein Transport; Rats; Urea Transporters; Urine; Vasopressins; Water-Electrolyte Imbalance

Heart failure is a leading cause of morbidity and mortality. In the United States, there are more than 5 million patients with heart failure and over 500,000 newly diagnosed cases each year. Numerous advances have been made in our understanding of the pathophysiologic mechanisms contributing to sodium and water retention in this condition. Important alterations in the sympathetic nervous system and the renin-angiotensin-aldosterone system have been described in heart failure, allowing the use of mechanism-specific treatments such as beta-adrenergic receptor antagonism and angiotensin-converting enzyme inhibition. As our understanding of the roles of the natriuretic peptides and the arginine vasopressin-aquaporin-2 system in the pathophysiology of heart failure evolves, treatments directed toward the alterations in these systems in heart failure can be further developed.

Topics: Adrenergic beta-Antagonists; Angiotensin-Converting Enzyme Inhibitors; Atrial Natriuretic Factor; Body Fluids; Heart Failure; Humans; Natriuretic Peptide, Brain; Neurosecretory Systems; Renin-Angiotensin System; Sodium; Sympathetic Nervous System; Vasopressins; Water Intoxication; Water-Electrolyte Imbalance

Topics: Acute Disease; Aquaporins; Brain Edema; Chronic Disease; Humans; Hyponatremia; Hypovolemia; Vasopressins; Water-Electrolyte Imbalance

Mechanisms by which luteinizing hormone-releasing hormone (LHRH) affects vasopressin secretion were investigated using the isolated rat hypothalamo-neurohypophysial explants. LHRH in a concentration of 4 x 10(-7)M inhibited both the basal and K(+)-stimulated vasopressin release from explants isolated from euhydrated rats. When, however, the tissue was obtained from animals previously salt-loaded, the inhibitory effect of LHRH was completely abolished, thus implying a decrease in the sensitivity to LHRH. LHRH did not affect vasopressin secretion under conditions of generalized blockade of synaptic inputs by 15 mM MgSO(4), suggesting the indirect action of this neurohormone on the hypothalamic magnocellular system. It is concluded that LHRH may play the role of a neuromodulator of vasopressinergic neurones in the rat.

Topics: Angiotensin II; Animals; Gonadotropin-Releasing Hormone; Hypothalamo-Hypophyseal System; In Vitro Techniques; Magnesium Sulfate; Male; Neurons; Potassium; Rats; Rats, Wistar; Sodium Chloride; Stimulation, Chemical; Synaptic Transmission; Vasoconstrictor Agents; Vasopressins; Water-Electrolyte Imbalance

Elevations of arginine vasopressin (AVP) binding to renal vasopressin V2 receptors (V2R) enhance water and urea reabsorption in the collecting duct epithelium. This study was designed to quantify the levels of V2R mRNA and protein within the distinct regions of the Sprague-Dawley rat kidney (i.e., the cortex and outer and inner medulla) during 24 and 48 h of water restriction. A competitive reverse transcription-polymerase chain reaction (RT-PCR) assay was developed to quantify changes in the V2R mRNA, in which a deletion mutant RNA transcript was used to control for the efficiency of RT-PCR. Western blot analysis was utilized for the quantification of the V2R protein. The results showed that the steady-state levels of the V2R mRNA decreased in a time-dependent manner in the cortex and outer and inner medulla throughout 48 h of water restriction. Western blot analysis revealed that the V2R protein in the renal cortex decreased after the initial 24 h of water restriction and remained decreased at 48 h. In contrast, outer medullary V2R protein decreased significantly only after 48 h of water restriction, whereas no significant change in the inner medullary V2R protein was observed throughout the 48 h of water restriction. These results suggest that water restriction leads to a regional time-dependent downregulation of the V2R mRNA and protein within the rat kidney. The stability of the plasma membrane V2R protein within the inner medulla may allow for the optimization of urine concentration and minimize water loss during periods of water restriction.

Topics: Animals; Kidney; Male; Polymerase Chain Reaction; Rats; Rats, Sprague-Dawley; Receptors, Vasopressin; RNA, Messenger; Signal Transduction; Time Factors; Vasopressins; Water; Water-Electrolyte Imbalance

Chronic schizophrenic patients are reported to develop imbalanced water homeostasis by the pathological secretion of vasopressin and aldosterone. We measured plasma vasopressin, aldosterone and atrial natriuretic peptide in schizophrenic patients to elucidate the role of these hormones during a perioperative period. Eighteen schizophrenic patients with chronic antipsychotic drugs over 10 years and 22 as a control group who underwent elective lower abdominal surgery were the subjects of this study. In the schizophrenic patients, plasma aldosterone secretion was significantly inhibited, while plasma vasopressin and atrial natriuretic peptide were significantly increased during surgery. A good relationship (r = 0.69, p < 0.01) between plasma atrial natriuretic peptide and plasma osmolality was obtained 60 min after skin incision, but not before the induction of anesthesia. The findings suggest that chronic schizophrenic patients may develop an abnormal secretion of vasopressin, aldosterone and atrial natriuretic peptide during anesthesia.

Topics: Adult; Aged; Aldosterone; Atrial Natriuretic Factor; Case-Control Studies; Chronic Disease; Dopamine; Female; Humans; Intraoperative Period; Linear Models; Male; Middle Aged; Osmolar Concentration; Prospective Studies; Schizophrenia; Time Factors; Vasopressins; Water-Electrolyte Imbalance

Hyponatremia after pituitary surgery is presumed to be due to antidiuresis; however, detailed prospective investigations of water balance that would define its pathophysiology and true incidence have not been established. In this prospective study, the authors documented water balance in patients for 10 days after surgery, monitored any sodium dysregulation, further characterized the pathophysiology of hyponatremia, and correlated the degree of intraoperative stalk and posterior pituitary damage with water balance dysfunction. Ninety-two patients who underwent transsphenoidal pituitary surgery were studied. To evaluate posterior pituitary damage, a questionnaire was completed immediately after surgery in 61 patients. To examine the osmotic regulation of vasopressin secretion in normonatremic patients, water loads were administered 7 days after surgery. Patients were categorized on the basis of postoperative plasma sodium patterns. After pituitary surgery, 25% of the patients developed spontaneous isolated hyponatremia (Day 7 +/- 0.4). Twenty percent of the patients developed diabetes insipidus and 46% remained normonatremic. Plasma arginine vasopressin (AVP) was not suppressed in hyponatremic patients during hypoosmolality or in two-thirds of the normonatremic patients after water-load testing. Only one-third of the normonatremic patients excreted the water load and suppressed AVP normally. Hyponatremic patients were more natriuretic, had lower dietary sodium intake, and had similar fluid intake and cortisol and atrial natriuretic peptide (ANP) levels compared with normonatremic patients. Normnonatremia, hyponatremia, and diabetes insipidus were associated with increasing degrees of surgical manipulation of the posterior lobe and pituitary stalk during surgery. The pathophysiology of hyponatremia after transsphenoidal surgery is complex. It is initiated by pituitary damage that produces AVP secretion and dysfunctional osmoregulation in most surgically treated patients. Additional events that act together to promote the clinical expression of hyponatremia include nonatrial natriuretic peptide-related excess natriuresis, inappropriately normal fluid intake and thirst, as well as low dietary sodium intake. Patients should be monitored closely for plasma sodium, plentiful dietary sodium replacement, mild fluid restriction, and attention to symptoms of hyponatremia during the first 2 weeks after transsphenoidal surgery.

Topics: Adult; Arginine Vasopressin; Atrial Natriuretic Factor; Child; Diabetes Insipidus; Diuresis; Female; Fluid Therapy; Humans; Hydrocortisone; Hyponatremia; Incidence; Intraoperative Complications; Male; Natriuresis; Pituitary Diseases; Pituitary Gland; Pituitary Gland, Posterior; Postoperative Complications; Prospective Studies; Renal Agents; Sodium; Sodium, Dietary; Sphenoid Bone; Thirst; Vasopressins; Water; Water-Electrolyte Balance; Water-Electrolyte Imbalance

The purpose of this report is to determine the mechanisms that lead to hyponatremia when isotonic saline was the only fluid infused into rats given antidiuretic hormone (ADH), and what might minimize the degree of this hyponatremia. Normal rats were deprived of food and water for the 24-hr study period. They received an infusion of isotonic saline to expand their extracellular fluid (ECF) volume with and without exogenous ADH administration (N = 8 in each of the four groups). Similar studies were also carried out in 32 rats fed a low electrolyte diet for 72 hr before the experiment. An additional control group was fed the low electrolyte diet supplemented with sodium (Na), potassium (K), and chloride (Cl). Hyponatremia developed over 24 hr in rats fed their usual diet if treated with ADH and isotonic saline (fall, 13 +/- 2 mM, P < 0.01). The hyponatremia was caused by negative balance for Na + K salts. Hyponatremia did not develop after the saline + ADH treatment if rats were pretreated for 3 days with a low electrolyte diet. Two factors were required to develop this hyponatremia--generation of electrolyte-free water as a result of the excretion of a large quantity of Na + K salts at a high concentration in the urine, and prevention of the excretion of this electrolyte-free water by ADH. Increasing the avidity for Na reabsorption by the kidney prevented this type of hyponatremia from developing.

Topics: Animals; Hyponatremia; Isotonic Solutions; Male; Rats; Rats, Wistar; Renal Agents; Sodium Chloride; Sodium Chloride, Dietary; Vasopressins; Water-Electrolyte Imbalance

Symptoms and other abnormalities associated with serum sodium imbalance were studied in bedridden elderly and healthy elderly subjects. 1. A significantly higher number of the bedridden elderly suffered from chronic wasting disease. 2. The average serum sodium concentration in bedridden elderly subjects was significantly lower than in healthy subjects, as was the sodium intake and the sodium content in urine, which indicate that the bedridden elderly subjects suffered from chronic sodium deficiency. 3. The bedridden elderly subjects had high levels of plasma PRA and antidiuretic hormone, and their aldosterone levels were low, which indicate that their condition was associated with a decrease in available circulating plasma, hypersecretion of antidiuretic hormone, and a decline in the ability to retain sodium. 4. Measurement of 24-hr creatinine clearance, albumin, and beta 2-microglobulin in urine revealed that bedridden elderly subjects had high levels of renal dysfunction, the result of which may a disturbance in water excretion. Abnormalities in serum sodium levels in the bedridden elderly subjects were related to a chronic deficiency in sodium intake, which reduced their ability to maintain sodium levels and impaired their renal function. Iatrogenic factors are likely to play an important role in the genesis of this condition, and should be taken into account in during management.

Topics: Aged; Bed Rest; Female; Fluid Therapy; Humans; Iatrogenic Disease; Kidney Diseases; Male; Sodium; Vasopressins; Water-Electrolyte Imbalance

Torsade de pointes is an unusual life-threatening ventricular arrhythmia that has been associated with vasopressin, neuroleptic drugs, and electrolyte imbalances, including hypokalemia and hypomagnesemia. Over a 9-month period, we observed torsade de pointes in three patients with cirrhosis and bleeding esophageal varices who did not have prior cardiac disease. All had received endoscopic sclerotherapy and continuous infusions of vasopressin and nitroglycerin. For sedation, two patients received haloperidol and one droperidol. In addition, two patients had either hypokalemia or hypomagnesemia. In all three patients, there was prolongation of the electrocardiographic QT interval and a "long-short" initiating sequence followed by ventricular tachycardia with torsade de pointes morphology. All were successfully cardioverted; there was one late death due to aspiration and septicemia. We conclude that cirrhotics with variceal hemorrhage may be at increased risk of developing this arrhythmia in the setting of treatment with vasopressin, sedation with neuroleptic drugs, and electrolyte abnormalities. We urge close monitoring of these patients for cardiac arrhythmia and recommend that neuroleptics be used cautiously, if at all.

Topics: Adult; Antipsychotic Agents; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Liver Cirrhosis; Male; Middle Aged; Torsades de Pointes; Vasopressins; Water-Electrolyte Imbalance

We evaluated the dynamic response of renin, aldosterone, and vasopressin to intravenous water loading (20 ml 5% glucose/kg b.w.) in 12 children (aged 7-18 years) with postinflammatory liver cirrhosis after hepatitis B virus (HBV) infection. All of the patients had early-stage liver cirrhosis; according to Child's classification, nine patients had group A; three, group B cirrhosis. A group of 17 children with chronic persistent hepatitis served as the control. The diagnoses were confirmed in all of the patients by liver biopsy. The patients followed a diet containing 3 mmol NaCl/kg/day, maximum 100 mmol per day for 6 days. Water loading was performed in recumbency over approximately 45 min. Renin, aldosterone, and vasopressin, assayed by radioimmunoassay (RIA), were determined before, 1 h, and 5 h after starting the water load. Prestudy hormone levels were within normal range in both groups. Renin and aldosterone concentration change patterns were similar in both groups and characterized by suppression of hormone activity caused by central volume expansion and recovery to prestudy levels after 5 h. However, the pattern of change of vasopressin concentrations differed in the control and study groups. In contrast to that of the controls, volume expansion did not suppress vasopressin in the group with liver cirrhosis. We conclude that failure to suppress vasopressin activity after central volume expansion may be one of the early mechanisms responsible for water-electrolyte imbalance in liver cirrhosis in children.

Topics: Adolescent; Aldosterone; Child; Female; Glucose; Hepatitis B; Humans; Infusions, Intravenous; Liver Cirrhosis; Male; Potassium; Renin; Renin-Angiotensin System; Sodium; Vasopressins; Water; Water-Electrolyte Imbalance

Controversial results of fluid and electrolyte derangements in patients with moderate alcohol intoxication have been described. However, no information is available about severe alcohol intoxication. We investigated differences of hormonal disorders between alcohol-habituated and alcohol-naive subjects with severe ethanol intoxication. The hormonal derangements and recommendations on therapy of these patients are discussed. Thirty-three patients [10 alcohol-naive (group A) and 23 alcohol-habituated (group B) subjects] with severe alcohol intoxication (blood ethanol > 200 mg/dl) were selected for the study. Electrolytes and osmolarity of serum and urine, blood ethanol, vasopressin, renin, and aldosterone were determined on admission 2, 4, and 6 hr later. Fluid balance was calculated for each hour. All patients received isotonic saline solution according to urine production. Group A: On admission, serum osmolarity was increased (308 mOsmol/kg). Concomitantly, vasopressin level was elevated on admission (9.12 pg/ml). Increased serum osmolarity was correlated with elevated vasopressin levels (r = 0.8211; p < 0.005). Serum electrolytes, renin, and aldosterone values were within normal ranges. Group B: On admission, vasopressin level was significantly decreased (0.9 pg/ml), despite an elevated serum osmolarity (309 mOsmol/kg). Serum osmolarity remained high despite a sufficient fluid substitution. In addition, vasopressin level remained suppressed over the observation period. Aldosterone level was significantly increased on admission (319 ng/ml). Accordingly, serum sodium was increased from 142 to 148 mM/liter, and serum potassium was decreased from 3.9 to 3.4 mM/liter. Response to hyperosmolarity due to severe alcohol intoxication is different in alcohol-naive and alcohol-habituated subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adolescent; Adult; Alcoholic Intoxication; Alcoholism; Aldosterone; Ethanol; Female; Humans; Kidney Function Tests; Male; Middle Aged; Potassium; Renin; Sodium; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Hypernatremia was detected in a dog that was evaluated because of seizures. During hospitalization, the dog was fully conscious and remained hypernatremic when drinking voluntarily and when water was added to the food. Urine volume increased and urine osmolality decreased during an infusion of hypertonic saline (2.5% NaCl) solution, despite development of progressive hyperosmolality. There was no correlation between plasma antidiuretic hormone concentration and osmolality during the infusion study. The dog released antidiuretic hormone normally after nonosmotic stimulation (ie, apomorphine administration). These findings allowed a diagnosis of hypodipsic hypernatremia caused by destruction of hypothalamic osmoreceptors. At necropsy, there was hydrocephalus, atrophy of the septum pellucidum, and neuraxonal dystrophy of the cuneate nuclei. The underlying neurologic disease responsible for the CNS lesions could not be determined, but hydrocephalus may have led to pressure atrophy in the region of the hypothalamus that contains osmoreceptors.

Topics: Animals; Brain Diseases; Dog Diseases; Dogs; Drinking; Fluid Therapy; Hypernatremia; Hypothalamus; Male; Osmolar Concentration; Seizures; Vasopressins; Water-Electrolyte Imbalance

We were interested to discover whether microglia could play a role in the remodelling of the adult CNS or participate in adaptations to physiological rather than pathological changes. We have studied microglia in the neurohypophysis of adult mice since microglia normally interact with neurons in this tissue and the biochemical and anatomical consequences of osmotic stress on the neurohypophysis are well known. In this study, we have examined microglial immuno-phenotype and numbers synthesizing DNA in the neurohypophysis of adult mice to establish whether these cells respond to progressive osmotic stress. Neurohypophyseal F4/80+ microglia underwent a large synchronous burst of DNA synthesis 48 h after initiation of osmotic stress (drinking 2.5% saline). The labelling index (percentage of F4/80+ cells labelled by [3H]thymidine) 1 h after injection the isotope rose to 17% from a control value of less than 1%. On the third day of treatment the labelling index had returned to control levels. In contrast, non-microglia cells in the neurohypophysis and microglial cells elsewhere in the brain did not show this response. The increase in DNA synthesis was not accompanied by signs of microglia activation commonly observed in inflammatory models. They did not acquire an "activated" or "hypertrophic" morphology, nor was their staining with a panel of antibodies greatly altered. A small up-regulation of CD45 expression was the only phenotypic change detected. Thus, neurohypophyseal microglia respond to increased neurosecretory activity during the adaptation to osmotic stress in a distinctive way which differs from microglia reactions to inflammatory stimuli elsewhere in the CNS.

Topics: Adaptation, Physiological; Animals; DNA; Female; Leukocyte Common Antigens; Mice; Mice, Inbred BALB C; Microglia; Osmotic Pressure; Pituitary Gland, Posterior; Saline Solution, Hypertonic; Vasopressins; Water-Electrolyte Imbalance

Previous studies have shown that common bile duct ligation in the rabbit is followed by a reduction of the extracellular water compartment. To further elucidate the mechanisms leading to volume depletion in this model, water and sodium balances and changes in plasma concentrations of atrial natriuretic peptide (ANP), vasopressin (ADH), plasma renin activity (PRA) and aldosterone (Ald) were investigated during the first 4 days after common bile duct ligation (group OJ,) or sham operation (group SO). Water and chow intakes were lower in group OJ (148 +/- 30 versus 226 +/- 40 mL/4 days; p = 0.004 and 12 +/- 9 versus 171 +/- 40 g/4 days; p = 0.0001). There were no differences in urine output. Sodium urinary losses were marginally higher in group OJ (12.4 +/- 7 versus 6.7 +/- 5 mEq/4 days; p = 0.06). Water balance was lower in group OJ (-50 +/- 56 versus 101 +/- 71 mL/4 days; p = 0.0001). At 24 hours, plasma ANP (41 +/- 7 versus 10.7 +/- 1 fmol/mL, p = 0.0001), ADH (21.8 +/- 7 versus 12.3 +/- 6 pg/mL, p = 0.008) and Ald (14.5 +/- 5 versus 3.7 +/- 3 ng/dL, p = 0.001) were higher in group OJ. These alterations persisted 72 hours after bile duct ligation, when a concomitant increase in PRA (10.7 +/- 5 versus 3 +/- 1.6 ng/dL, p = 0.006) was also observed. A group of pair-fed pair-watered sham-operated controls (group SO2, n = 13) showed a metabolic profile similar to group OJ but a low ANP concentration. Multiple venous sampling in five rabbits 24 hours after bile duct ligation showed the highest plasma levels of ANP in the aorta and infrarenal vena cava. These results suggest that common bile duct ligation in the rabbit is followed by marked hypodipsia and hypophagia, possibly mediated by ANP, leading to isotonic volume depletion and secondary activation of the water and sodium retaining hormones.

Topics: Acute Kidney Injury; Aldosterone; Animals; Atrial Natriuretic Factor; Cholestasis; Common Bile Duct; Ligation; Male; Natriuresis; Rabbits; Renin; Time Factors; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

It is commonly taught that retention of free water is the dominant factor reducing the serum sodium concentration in hyponatremia. To determine whether the concentrations of other electrolytes are similarly diluted, we identified 51 patients with hyponatremia (Na = 121 +/- 1 mmol/L [mEq/L]) and compared electrolyte and laboratory values at the time of hyponatremia with values at a time when serum sodium was in the normal range (138 +/- 1 mmol/L). The medium interval between these measurements was 12 days. At the time of hyponatremia, serum sodium and chloride were substantially and significantly reduced by 12% to 15%. Although many hyponatremic patients had overtly increased or decreased concentrations of the other measured electrolytes, there were no significant changes in the mean concentration for any of these at the time of hyponatremia. Unchanged mean values were found for the plasma concentration of bicarbonate (26.1 +/- 0.6 normal v 25.2 +/- 0.8 mmol/L at the time of hyponatremia), potassium (4.31 +/- 0.10 v 4.33 +/- 0.15 mmol/L), albumin, phosphate, and creatinine. The stability of these laboratory values was observed both in patients with clinically normal extracellular fluid (ECF) volume and in those with true or effective ECF depletion. The urinary sodium (UNa) concentration was found to be a reliable predictor of the ECF volume status, whereas the fractional sodium excretion (FENa) was not. Electrolyte derangements are common in patients with hyponatremia, but are usually confined to patients on diuretics or who have an abnormal ECF volume. In the absence of these complicating situations, the plasma electrolytes are typically normal and are not reduced by dilution to the same extent as Na and CI. Based on a review of both the classic and recent knowledge concerning electrolyte regulation in hyponatremia, we propose that two factors explain these observations. First, the degree of dilution is overestimated because of Na losses in urine and perhaps Na shift into cells. Second, both renal and extrarenal adaptive mechanisms are activated by hyponatremia that stabilizes the concentration of other ions. One of these mechanisms is cell swelling, which triggers a volume-regulatory response leading to the release of ions and water into the ECF. Other adaptive mechanisms are mediated by antidiuretic hormone (ADH) per se, and by atrial natriuretic peptide (ANP).

Topics: Adaptation, Physiological; Animals; Atrial Natriuretic Factor; Bicarbonates; Extracellular Space; Humans; Hyponatremia; Incidence; Potassium; Retrospective Studies; Urea; Uric Acid; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

The case of a 30-year-old pregnant patient suffering from panhypopituitarism is presented. Pregnancy induced by HMG/HCG had been uneventful. Induction of labor by PGE2 vaginal tablets and by intravenous oxytocin at 42 gestational weeks failed and the patient was operated. Following the operation severe exacerbation of her diabetes insipidus occurred. Fluid balance mechanism failed and electrolyte status deteriorated rapidly. The importance of pitressin in maintenance of fluid and electrolyte balance in panhypopituitaric patients in labor and surgical trauma is stressed.

Topics: Adult; Female; Fluid Therapy; Humans; Hydrocortisone; Hypopituitarism; Labor, Induced; Prednisone; Pregnancy; Pregnancy Complications; Thyroxine; Vasopressins; Water-Electrolyte Imbalance

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

Water retention in cirrhosis has classically been considered to be due to a low distal fluid delivery secondary to increased proximal sodium reabsorption. However, recent studies showing high plasma vasopressin levels in patients and rats with cirrhosis, ascites, and dilutional hyponatremia suggest that a nonosmotic vasopressin hypersecretion could be an alternative mechanism. To investigate the role of vasopressin in water retention in cirrhosis, the renal ability to excrete a water load (50 ml/kg body wt), as estimated by the minimum urinary osmolality and the percentage of the water load excreted during 3 h, was assessed in 10 control rats and in 20 cirrhotic rats with ascites and impaired water excretion and high urinary excretion of vasopressin. Twenty-four hours later, the same procedure was repeated in cirrhotic rats 20 min after the subcutaneous injection (30 micrograms/kg body wt) of d(CH2)5Tyr(Et) VAVP, an antagonist of the hydroosmotic effects of vasopressin (10 rats), or the vehicle (10 rats). Treatment with the vasopressin antagonist normalized water excretion in 9 of the 10 rats. No significant changes in renal water metabolism were observed in the group of rats given the vehicle. These results indicate that vasopressin hypersecretion is the predominant mechanism of the impairment in water excretion in rats with experimental cirrhosis and ascites.

Topics: Animals; Arginine Vasopressin; Diuresis; Kidney; Liver Cirrhosis, Experimental; Male; Rats; Rats, Inbred Strains; Vasopressins; Water-Electrolyte Imbalance

Topics: Diabetes Insipidus; Humans; Polyuria; Vasopressins; Water-Electrolyte Imbalance

Topics: Aged; Humans; Hypernatremia; Male; Thirst; Vasopressins; Water-Electrolyte Imbalance

Although controlled mechanical ventilation (CMV) with positive end-expiratory pressure (PEEP) has a central place in the treatment of acute respiratory failure (ARF), several side effects of this technique have to be faced. CMV with PEEP may induce pulmonary barotrauma, disturbance of cardiac performance, impairment of renal function and fluid retention. Atrial natriuretic peptides (ANP) are released from the atria upon stretching and play a major role in the control of sodium and fluid balance. Therefore it was logical to determine plasma levels of alpha-ANP in CMV. A study performed in 7 patients suffering from ARF suggested that alpha-ANP plasma levels were depressed during PEEP at 15 cm H2O in comparison with PEEP at 0 cm H2O (ZEEP). The decrease in plasma levels of alpha-ANP was evident in samples taken from superior vena cava, right atrium, pulmonary artery and radial artery as well. The decrease in alpha-ANP was associated with a decline in cardiac index, creatinine clearance, urinary output and urinary sodium excretion. Experiments in volume- expanded healthy volunteers also suggest that CMV with PEEP is able to depress plasma levels of alpha-ANP. The reasons behind the decline in release of alpha-ANP may be atrial compression by the distended lungs and the well-known reduction of venous return to the heart. Other possible factors promoting fluid retention during CMV with PEEP are the decrease in cardiac index and glomerular filtration rate, changes in intrarenal distribution of blood flow, and a stimulation of release of antidiuretic hormone via stretch receptors in the left atrium and baroreceptors in aorta and carotid arteries.

Topics: Animals; Atrial Natriuretic Factor; Humans; Kidney; Positive-Pressure Respiration; Respiratory Distress Syndrome; Vasopressins; Water-Electrolyte Imbalance

Topics: Heart Failure; Humans; Kidney; Renin-Angiotensin System; Sodium; Vasopressins; Water-Electrolyte Imbalance

Topics: Adult; Aged; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Vasopressins; Water-Electrolyte Imbalance

Topics: Animals; Blood Volume; Diabetes Mellitus; Glomerular Filtration Rate; Hemodynamics; Kidney; Male; Plasma Volume; Rats; Rats, Brattleboro; Rats, Inbred Strains; Vasopressins; Water-Electrolyte Imbalance

Topics: Humans; Inappropriate ADH Syndrome; Vasopressins; Water-Electrolyte Imbalance

Topics: Child; Diabetes Insipidus; Humans; Osmolar Concentration; Vasopressins; Water-Electrolyte Imbalance

Hyponatremia developing some days after transsphenoidal pituitary adenectomy is a treacherous complication of uncertain cause. Of 19 patients monitored in a pilot study at the Wessex Neurological Centre, plasma sodium fell below 125 mmol/liter in three patients at times ranging from 6 to 9 days postoperatively. One patient had evidence of inappropriate secretion of arginine vasopressin (AVP), and the other two probably had steroid insufficiency despite apparently adequate steroid cover. In a more detailed study, the fluid and sodium balance of a further 16 patients was monitored for 7 to 11 days following transsphenoidal surgery together with plasma cortisol, renin, and AVP concentrations. No patient became severely hyponatremic. Three developed partial diabetes insipidus. Two patients with Cushing's disease had evidence of postoperative corticosteroid insufficiency despite normal steroid protection. An inappropriately low plasma cortisol concentration was recorded in both. Plasma AVP concentrations did not show a delayed surge postoperatively. Delayed hyponatremia appears to occur most often in patients with hypoadrenalism, as glucocorticoid cover is decreased. It results from water retention combined with natriuresis, and is reversed by glucocorticoid treatment.

Topics: Adenoma; Adult; Arginine Vasopressin; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Pituitary Neoplasms; Vasopressins; Water-Electrolyte Imbalance

Topics: Biological Transport, Active; Body Fluids; Body Water; Capillary Permeability; Edema; Electrolytes; Extracellular Space; Humans; Kidney Concentrating Ability; Kidney Glomerulus; Nephrons; Urine; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Early alterations in fluid, electrolytes, and their regulating hormones were investigated in men exposed to 6,000 m simulated altitude (2 h-ascent, 2 h-sojourn, 2 h-return). Hematocrit and serum protein rose with elevated serum osmolality and reduced urine flow upon arrival at 6,000 m, suggesting decreased plasma volume probably due to hypotonic fluid shift to intracellular spaces. Serum K declined reflecting respiratory alkalosis. The exposure raised plasma antidiuretic hormone (ADH), plasma renin activity (PRA), serum cortisol and aldosterone. Increases both in ADH and aldosterone showed close correlations with that in cortisol, suggesting that ADH may be elevated by hypoxic stress in addition to elevated serum osmolality and decreased plasma volume, and that increased secretion of adrenocorticotropin may be the main cause of increased aldosterone, though PRA involvement cannot be excluded. These rises in ADH and aldosterone may act to retain body water, and the latter may exaggerate alkalosis; thus, these hormonal changes may be related to acute mountain sickness.

Topics: Adult; Aldosterone; Altitude; Altitude Sickness; Atmosphere Exposure Chambers; Blood Proteins; Female; Hematocrit; Hormones; Humans; Hydrocortisone; Male; Middle Aged; Osmolar Concentration; Potassium; Renin; Urine; Vasopressins; Water-Electrolyte Imbalance

Hyponatremia and hypo-osmolality developed in a 70-year-old patient. It was probably mediated by hypersecretion of antidiuretic hormone, which, in turn, was due to prolonged nausea and vomiting. Severe esophagitis was the cause of the nausea. The patient was not given large amounts of fluids intravenously, and it is likely that she continued to drink for nondipsetic reasons. In view of her medical history of neurosyphilis, the possibility of a disturbance in the mechanism of thirst regulation is discussed, but remains unproved.

Topics: Aged; Esophagitis, Peptic; Female; Humans; Hyponatremia; Nausea; Osmolar Concentration; Syndrome; Time Factors; Vasopressins; Vomiting; Water-Electrolyte Imbalance

To verify whether or not an increased secretion of ADH may cause the water retention commonly observed in nephrotic syndrome, 16 nephrotic patients and 13 normal control subjects were studied in basal conditions and following a water load or an iso-osmotic blood volume expansion by 20% albumin infusion. In the basal condition there were no differences in plasma ADH, urine output, urinary osmolality (UOsm), and plasma renin activity between nephrotic patients and control subjects; POsm, PNa+, UNaV, and blood volume (BV) instead, were significantly lower in nephrotic patients than in control subjects. Following the water load control subjects reached a minimal UOsm of 82 +/- 12 mOsm/kg at 60 min and excreted completely the ingested water in 150 min; nephrotic patients reached a minimal UOsm of 160 +/- 111 mOsm/kg at 120 min, and the water was eliminated completely in 240 min. Plasma ADH decreased significantly in the first hour following water load only in control subjects. A significant direct correlation was observed between plasma ADH and POsm in control subjects (ADH = -85 + 0.30 POsm, P less than 0.001) but not in nephrotic patients. Plasma ADH was inversely correlated with BV in nephrotic patients (ADH = 15.47 -0.17 BV, P less than 0.001) but not in normal control subjects. In nephrotic patients with reduced BV the expansion of BV with 20% albumin was effective in reducing the plasma levels of ADH and promoting a water diuresis. Our results demonstrate a sustained volume mediated secretion of ADH in the nephrotic syndrome, which is responsible for the impairment in water excretion.

Topics: Adolescent; Adult; Blood Volume; Child; Female; Glomerulonephritis; Hematuria; Humans; Male; Middle Aged; Nephrotic Syndrome; Osmolar Concentration; Vasopressins; Water-Electrolyte Imbalance

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

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

Plasma vasopressin was measured before and after tilt testing in 18 patients with orthostatic hypotension of various causes. In six patients, all of whom had normal osmotic regulation of vasopressin, normal stimulation of vasopressin did not occur on tilt testing; all six had clinical evidence of defects in the afferent or central connections of the baroregulatory reflex arc. In the remaining 12 patients, plasma vasopressin increased to levels appropriate for the degree of hypotension; none of these patients had clinical evidence of defects in afferent or central portions of the baroregulatory arc. Those with subnormal vasopressin response had significantly more severe orthostatic hypotension than the patients with normal vasopressin response, but none had plasma hypotonicity, an abnormality present in one-quarter of those with normal response. It is concluded that the vasopressin response to orthostatic hypotension may serve as a test of the integrity of the afferent and central components of the baroregulatory reflex arc. Furthermore, this study suggests that the normal vasopressin response to orthostatic hypotension may moderate the fall in blood pressure but may adversely affect water balance.

Topics: Adult; Aged; Female; Hemodynamics; Humans; Hypotension, Orthostatic; Male; Middle Aged; Norepinephrine; Pressoreceptors; Sympathetic Nervous System; Vasopressins; Water-Electrolyte Imbalance

Topics: Animals; Diabetes Insipidus; Diuresis; Female; Glomerular Filtration Rate; Hydronephrosis; Kidney; Male; Osmolar Concentration; Rats; Rats, Brattleboro; Rats, Mutant Strains; Sex Factors; Vasopressins; Water-Electrolyte Imbalance

Topics: Animals; Arginine Vasopressin; Body Water; Deamino Arginine Vasopressin; Diabetes Insipidus; Diuresis; Drinking; Hypothalamus; Osmolar Concentration; Pituitary Gland, Posterior; Rats; Rats, Brattleboro; Rats, Mutant Strains; Thirst; Vasopressins; Water-Electrolyte Imbalance

Seven subjects with Kallmann's syndrome were studied to determine whether they had disturbances of fluid homeostasis. Simultaneous measurements of urine and plasma osmolality (Uosm and Posm, respectively) were made during free access to fluids. The Uosm-Posm relationship was abnormal in five patients on at least one occasion. Patient 2 was frequently overhydrated (Posm less than or equal to 280 mosmol/kg) and patient 5 excreted a dilute urine when his Posm was 290 mosmol/kg. The three subjects (1, 5, and 7) tending to have an increased Psom (greater than or equal to 300 mosmol/kg) were able to concentrate their urine (Uosm greater than 800 mosmol/kg) and denied polyuria and polydipsia. Their elevated Posms could be explained by impairment of thirst, rather than increased excretion of water, because the patients concentrated their urines at normal Posms during fluid deprivation. The osmotic threshold for vasopressin release was decreased (Posm = 270.6 mosmol/kg) in one patient and increased (Posm greater than or equal to 295 mosmol/kg) in two others of the seven patients. The elevated osmotic threshold was not due to chronic hyperosmolality or a generalized defect in vasopressin secretion. In the patient with the highest osmotic threshold (Posm = 296 mosmol/kg) and Posms between 289--301 mosmol/kg during free access to fluid, the osmotic threshold decreased to only 293 mosmol/kg after 6 weeks of adequate hydration and desmopressin acetate. However, in response to hypotension induced by trimethaphan, he increased his plasma vasopressin from 1--26 microU/ml. In conclusion, some patients with Kallmann's syndrome may have osmoreceptor dysfunction and abnormal thirst regulation, indicating more extensive hypothalamic involvement than previously appreciated.

Topics: Adolescent; Adult; Diuresis; Female; Humans; Hypogonadism; Male; Osmolar Concentration; Syndrome; Thirst; Trimethaphan; Vasopressins; Water Deprivation; Water-Electrolyte Imbalance

Topics: Adult; Body Fluids; Humans; Hypernatremia; Male; Posture; Sensory Receptor Cells; Vasopressins; Water-Electrolyte Imbalance

Plasma vasopressin was measured in seven insulin-treated diabetics during 24 h of insulin withdrawal to determine: 1) if abnormalities of the neurohypophysial-renal axis contribute to the dehydration of uncontrolled diabetes mellitus; and 2) the factors causing elevated levels of vasopressin in diabetic ketoacidosis. During the 24 h period of insulin withdrawal, blood glucose rose from 6.7 +/- 1.0 to 20.7 +/- 2.4 mmol/l, whereas plasma vasopressin was 3.6 +/- 0.5 pg/ml initially and in four patients showed little change. Markedly elevated levels of plasma vasopressin (17.8, 19.8 and 26.6 pg/ml) were observed in three patients following the onset of hypovolaemia, nausea and/or vomiting which are known to stimulate vasopressin release. Free water clearance was negative throughout the study in all patients. Thirst was not noted despite marked hyperglycaemia (16.9 +/- 2.5 mmol/l) until a significant fall in body weight of 0.9 +/- 0.2 kg had occurred (p less than 0.005). We concluded that marked elevation of vasopressin results from non-osmotic stimulation and that the mechanisms of body water conservation are overridden by the glycosuric diuresis.

Topics: Adult; Blood Glucose; Blood Pressure; Body Weight; Diabetes Mellitus; Female; Humans; Insulin; Male; Osmolar Concentration; Sodium; Vasopressins; Water-Electrolyte Imbalance

Serum osmolality and antidiuretic hormone (ADH) levels were determined for 17 patients with cerebral infarction, 4 with subarachnoid hemorrhage, and 12 controls. The ADH levels were elevated significantly in the stroke patients. Hyponatremia was not observed. Stroke patients are at risk for developing electrolyte disturbances; thus, fluid intake and electrolyte levels should be closely observed.

Topics: Cerebral Infarction; Humans; Inappropriate ADH Syndrome; Subarachnoid Hemorrhage; Vasopressins; Water-Electrolyte Imbalance

Topics: Arginine Vasopressin; Body Water; Deamino Arginine Vasopressin; Diabetes Insipidus; Humans; Hypernatremia; Hypoglycemia; Hyponatremia; Inappropriate ADH Syndrome; Pharmacology; Radioimmunoassay; Vasopressins; Water-Electrolyte Imbalance

To examine the weight loss of hyperbaric helium-oxygen habitation, we measured the exchange of liquids and calories in six men who lived in this atmosphere for 32 d. The maximum pressure was 49.5 ATA. The men lost 3.7-10.1 kg, in spite of warm ambient (31-32 degrees C) temperatures and adequate calories (2,737 kcal/d) provided for the sedentary ways of chamber living. Weight loss and a calculated fluid deficit were accompanied by significant hemoconcentration, shown by increases in serum proteins. These changes were followed by a rise in urinary aldosterone and vasopressin, but not thirst. Weight loss in hyperbaric atmospheres is probably multifactorial, but our data suggests an uncoupling of normal osmoregulation may have occurred in the present set of subjects. This may have been due to altered lung mechanics, increased catecholamines, or effects of high pressure on cellular responses to vasopressin.

Topics: Aldosterone; Atmospheric Pressure; Body Weight; Carbon Dioxide; Decompression; Diving; Extraterrestrial Environment; Humans; Oxygen Consumption; Time Factors; Vasopressins; Water-Electrolyte Imbalance

Topics: Demeclocycline; Female; Humans; Hyponatremia; Hypothyroidism; Inappropriate ADH Syndrome; Middle Aged; Vasopressins; Water-Electrolyte Imbalance

A double paraneoplasic syndrome with hypersecretion of ADH and ACTH revealed the presence of a small cell bronchial cancer in a man aged 62 years. Water and electrolyte anomalies due to the hypersecretions were of such a degree that an occlusive syndrome occurred. Very high levels of ADH and ACTH were found in the tumoral tissue. The measurement of these levels is rarely conducted at the present time but was able to define the mechanism of abnormal secretion of these two hormones in this case.

Topics: Adrenocortical Hyperfunction; Adrenocorticotropic Hormone; APUD Cells; Carcinoma; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Middle Aged; Paraneoplastic Syndromes; Vasopressins; Water-Electrolyte Imbalance

Topics: Aged; Dermatitis, Exfoliative; Humans; Male; Middle Aged; Vasopressins; Water-Electrolyte Imbalance

Following some remarks on the hyposomolar-hyponatraemic syndrome and on the formation of free water, the possible aetiopathogenetic mechanisms of hyponatraemia in ascitogenous cirrhosis of the liver and in particular the role of ADH are considered. 3 cases out of 18 suffering from ascitic phase cirrhosis in whom inability to produce free water was accompanied by conserved urinary excretion of sodium are reported. One explanation might be the intervention of ADH or of an antidiuretic substance.

Topics: Adult; Aged; Ascites; Female; Humans; Hyponatremia; Liver Cirrhosis; Male; Middle Aged; Osmolar Concentration; Vasopressins; Water-Electrolyte Imbalance

Sodium and water retention is constant in decompensated cirrhosis with ascites and edema. Sodium retention is due to several factors. Renal hemodynamic disturbances appear first: decrease in glomerular filtration and renal plasmatic perfusion, redistribution of renal perfusion to the juxtamedullar area where the longer nephrons reabsorb more sodium. Metabolic disorders of estrogens, natriuretic hormonal factor, prostaglandins and the kallikrein-kinin system contribute to greater sodium retention. Water retention is secondary to greater sodium reabsorption and to hyperactivity of the antidiuretic hormone. Sodium and water retention, associated with portal hypertension, with reduced oncotic pressure and with dynamic lymphatic insufficiency, is responsible for the production of ascites. The latter results in a decrease in the effective plasmatic volume, with non-suppression of the renin-angiotensin system, increased aldosterone production and additional sodium retention.

Topics: Ascites; Estrogens; Glomerular Filtration Rate; Humans; Kallikreins; Prostaglandins; Sodium; Vasopressins; Water-Electrolyte Imbalance

Topics: Adult; Body Water; Diabetes Insipidus; Diuresis; Extracellular Space; Humans; Hypernatremia; Hyponatremia; Inappropriate ADH Syndrome; Intracellular Fluid; Kidney Concentrating Ability; Kidney Failure, Chronic; Osmolar Concentration; Sodium; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Topics: Aldosterone; Calcium; Diabetes Insipidus; Electrolytes; Endocrine System Diseases; Humans; Parathyroid Diseases; Parathyroid Hormone; Sodium; Thyroid Diseases; Vasopressins; Water-Electrolyte Imbalance

Pontine myelinolysis can be suspected clinically on the basis of the following criteria: (1) Electrolyte disturbance manifested mainly by hyponatremia; (2) progressive neurologic deficits resulting in a "locked-in" syndrome; (3) usually, but not necessarily, alcohol abuse; and (4) frequent iatrogenic precipitation of the syndrome by inappropriate rehydration of patients at risk. A major pathophysiologic mechanism for this disorder seems to be the anatomic grid structure of the base of the pons, which is more vulnerable to edema than the cerebral hemispheres. Treatment should be focused on rapid reversal of electrolyte imbalance and judicious use of dehydrating agents. Early diagnosis and treatment might reverse an otherwise malignant syndrome.

Topics: Adolescent; Adult; Aged; Alcoholism; Brain Edema; Brain Stem; Child; Child, Preschool; Demyelinating Diseases; Female; Humans; Hyponatremia; Male; Middle Aged; Pons; Vasopressins; Water-Electrolyte Imbalance

Topics: Diseases in Twins; Humans; Hyponatremia; Hypothyroidism; Infant; Kidney; Male; Sodium; Syndrome; Vasopressins; Water-Electrolyte Imbalance

Topics: Humans; Osmolar Concentration; Vasopressins; Water-Electrolyte Imbalance

Topics: Adult; Female; Fluphenazine; Humans; Syndrome; Vasopressins; Water-Electrolyte Imbalance

Topics: Female; Humans; Middle Aged; Syndrome; Thioridazine; Vasopressins; Water-Electrolyte Imbalance

Topics: Child; Craniopharyngioma; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant; Male; Pituitary Neoplasms; Postoperative Care; Postoperative Complications; Sodium; Time Factors; Vasopressins; Water-Electrolyte Imbalance

Topics: Adrenal Gland Diseases; Adrenal Glands; Age Factors; Aged; Brain Edema; Female; Humans; Hyponatremia; Iatrogenic Disease; Kidney; Liver Cirrhosis; Male; Sodium; Vasopressins; Water-Electrolyte Imbalance

3 cases of inappropriate vasopressin secretion during one case of anaplastic carcinoma of the lung, one case of carcinoma of the prostate with bony metastases and one case of acute intermittent porphyria are presented. The plasma levels of vasopressin, measured by radioimmunoassay were high. Treatment with demeclocycline was attempted in one case. The clearance of free water was positive but the treatment was poorly tolerated by the digestive tract.

Topics: Acute Disease; Aged; Carcinoma; Demeclocycline; Female; Humans; Lung Neoplasms; Male; Paraneoplastic Endocrine Syndromes; Porphyrias; Prostatic Neoplasms; Syndrome; Vasopressins; Water-Electrolyte Imbalance

Topics: Angiography; Barium Sulfate; Counseling; Esophageal and Gastric Varices; Esophagoscopy; Gastrointestinal Hemorrhage; Hemostatic Techniques; Hepatic Encephalopathy; Humans; Hypertension, Portal; Medical History Taking; Physical Examination; Vasopressins; Water-Electrolyte Imbalance

Forty patients suffering from idiopathic oedema were studied. The disturbance in water excretion is characterised by a delay in excretion of a water load (20 ml/kg body weight), an inability to decrease urinary osmolarity below 137 mOsm/1 standing (normal: 60 mOsm +/- 25) and an inability to increase free water clearance: 2.36 +/- 2 ml/mn/1. 73 m2 (normal value: 6.8 ml/mn/1.73 m2) in the upright position. This problem of water excretion related to orthostasis defines and characterises the syndrome, the clinical picture of which is well known. The disturbance suggest a fault in the regulation of anti-diuretic hormone whilst the aldosteronism often described would seem to be inconstant and secondary to diuretic therapy too often prescribed without supervision.

Topics: Adult; Diuresis; Edema; Female; Humans; Male; Middle Aged; Osmolar Concentration; Posture; Syndrome; Vasopressins; Water-Electrolyte Imbalance

In 100 patients with different forms of cerebral strokes the author studied the general water content. Its distribution in the organism. Na and K concentration in the plasma and erythrocytes and the general electrolyte content in spaces of the body. It was established that the most frequent syndromes of water-electrolyte disorders in the acute period of strokes is intracellular or general hydratation (81%). In parenchymatous-subarachnoidal hemorrhages the general dehydratation was combined with a hyperhydratation of the extracellular space, while in sichemic strokes there was an anhydridemia up to 10-18 days. A disturbance of the electrolyte metabolism was also expressed in a transmineralization with a drop of the general Na and K content due to intracellular losses. The K deficit was averagely 29% and the Na--15.5% and should be taken into consideration in a substitutive hydro-electrolyte therapy. Solutions with an increased K content should be used in order to compensate its deficit.

Topics: Acute Disease; Adrenal Cortex; Body Water; Cerebral Hemorrhage; Cerebrovascular Disorders; Extracellular Space; Humans; Hypothalamus; Mineralocorticoids; Plasma Volume; Potassium; Sodium; Time Factors; Vasopressins; Water-Electrolyte Imbalance

A prospective study of bacterial meningitis in children was initiated two years ago. Serum sodium concentrations below 135 MEQ/liter were noted on admission in 72 of 124 (58.1 %) of patients enrolled in the study protocol. Low initial serum sodium concentration and prolonged depression in serum sodium despite fluid restriction correlated significanly (P less than 0.001 to 0.01) with the presence of neurologic sequelae of the disease. Inappropriate secretion of antidiuretic hormone as the cause of these electrolyte changes could be inferred by indirect measurement of serum and urine solute and volume data and was specifically documented, in patients enrolled most recently, by specific radioimmunoassay of antidiuretic hormone.

Topics: Adolescent; Child; Child, Preschool; Humans; Infant; Meningitis; Sodium; Vasopressins; Water-Electrolyte Imbalance

A case of a 76-year-old man with the syndrome of inappropriate secretion of antidiuretic hormone (ADH) is discussed. The patient was initially treated with fluid restriction followed by the administration of hypertonic saline. After failure to achieve rapid correction of the condition and continued lethargy and muscle weakness in the patient, a trial with lithium carbonate 300 mg three times daily via nasogastric tube was initiated. This resulted in a prompt reversal of the hyperosmolar state and improvement in electrolyte balance. However, despite the apparent success in treating his inappropriate ADH, the patient expired as a result of a massive cerebral vascular accident. The potential benefit of using lithium in the treatment of the syndrome of inappropriate secretion of ADH, and possible mechanisms of action, are reviewed.

Topics: Aged; Humans; Lithium; Male; Syndrome; Vasopressins; Water-Electrolyte Imbalance

Topics: Adrenalectomy; Animals; Body Weight; Calcium; Chlorides; Diabetes Insipidus; Drinking Behavior; Magnesium; Male; Potassium; Rats; Sodium; Urea; Vasopressins; Water-Electrolyte Imbalance

Topics: Anemia, Sickle Cell; Chronic Disease; Diabetes Insipidus; Diet; Humans; Hydrogen-Ion Concentration; Hypernatremia; Hyponatremia; Kidney; Kidney Concentrating Ability; Kidney Diseases; Osmolar Concentration; Vasopressins; Water-Electrolyte Imbalance

Topics: Adenocarcinoma, Bronchiolo-Alveolar; Aged; Demeclocycline; Humans; Lung Neoplasms; Male; Vasopressins; Water-Electrolyte Imbalance

Topics: Arginine Vasopressin; Blood Pressure; Blood Volume; Female; Humans; Hypothalamus; Male; Osmolar Concentration; Receptors, Cell Surface; Saline Solution, Hypertonic; Stimulation, Chemical; Thirst; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Four cases of cerebral edema associated with therapy for diabetic ketoacidosis are reported. One patient had an inappropriate ADH-like syndrome at the time of onset of clinical symptoms of cerebral edema; he survived. The remaining patients had hyponatremia at or near the time of onset of clinical symptoms of cerebral edema, and they subsequently died. The literature is reviewed and some aspects of therapy, which might be casually related to cerebral edema observed in association with therapy of diabetic ketoacidosis, are discussed.

Topics: Blood; Brain Edema; Child; Child, Preschool; Diabetic Ketoacidosis; Female; Hormones, Ectopic; Humans; Hyponatremia; Infusions, Parenteral; Insulin; Male; Osmolar Concentration; Vasopressins; Water-Electrolyte Imbalance

Topics: Analgesics; Antidepressive Agents, Tricyclic; Antineoplastic Agents; Arginine Vasopressin; Biguanides; Carbamazepine; Clofibrate; Diuretics; Humans; Kidney; Narcotics; Nicotine; Sulfonylurea Compounds; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Topics: Anemia, Sickle Cell; Child; Female; Humans; Hyponatremia; Syndrome; Vasopressins; Water-Electrolyte Imbalance

A 7-year-old girl twice developed severe hypernatremia (serum sodium values up to 194 mEq/l) without obvious cause. The ability of her kidneys to conserve water was normal, and increasing her plasma osmolality stimulated an appropriate ADH response. Unable to excrete a water load, her kidneys continued to conserve water even with a serum sodium concentration of 133 mEq/l. She was never thirsty and did not ingest sufficient fluid by choice. Although there was no demonstrable anatomic lesion, we postulate a localized defect of her thirst center. This may have modified release of ADH and resulted in an inability to dilute the urine by interrupting a pathway that could exist from the thirst center to the supraoptic nuclei. A therapeutic regimen based on these studies has prevented further hypernatremia.

Topics: Child; Child, Preschool; Drinking; Female; Glucose; Humans; Hypernatremia; Infusions, Parenteral; Recurrence; Saline Solution, Hypertonic; Thirst; Vasopressins; Water-Electrolyte Imbalance

When the extra-cellular fluid volume is expanded, the subsequent rise in urinary sodium excretion that occurs is due in part to a change in the concentration of some circulating natriuretic substance. Two natriuretic substances with different characteristics on Sephadex chromatography have been previously been identified separately by different workers. Extracts prepared from the urine of 31 normal subjects were tested for these two natriuretic materials in the normal conscious water-loaded rat. Two natriuretic fractions were found. The larger of the two was prepared on G50 Sephadex, and the smaller on G25 Sephadex. The natriuresis produced by the larger material was slow to develop and persisted for two hours. The natriuresis produced by the smaller material was maximal in the first 20 min, declined rapidly within the next 40 min, and tended to rise again during the subsequent 60 min. The amount of natriuretic activity that could be extracted from the freeze-dried urine was diminished by high concentrations of sodium chloride. The natriuretic activity of both materials was greater in the urine of the subjects when they were salt-loaded than when they were salt-depleted. The urine of salt-depleted subjects contained significant amounts of natriuretic material.

Topics: Animals; Chromatography, Ion Exchange; Creatinine; Diet, Sodium-Restricted; Humans; Male; Natriuresis; Rats; Sodium Chloride; Urine; Vasopressins; Water-Electrolyte Imbalance

Topics: Humans; Osmolar Concentration; Pituitary Diseases; Pituitary Gland, Posterior; Sensory Receptor Cells; Vasopressins; Water-Electrolyte Imbalance

Topics: Aldosterone; Edema; Humans; Vasopressins; Water-Electrolyte Imbalance

Topics: Female; Humans; Hyponatremia; Middle Aged; Osmolar Concentration; Sodium; Vasopressins; Water-Electrolyte Imbalance

Metabolic abnormalities compatible with inappropriate secretion of ADH developed during the course of severe viral pneumonia in a 17-year-old Navy recruit. With a regimen of strict fluid restriction, normalization of these abnormalities occurred. Marked leukopenia and hypoxia were also present, but gradually improved with resolution of the pneumonia. Inappropriate ADH secretion has been associated most often with bacterial pneumonia and this patient represents one of the few with viral pneumonia complicated by this syndrome. While the previous cases were assoicated with influenza virus, this patient was infected with adenovirus-7 which is endemic in the military recruit population.

Topics: Adenoviridae; Adenoviridae Infections; Adolescent; Hormones, Ectopic; Humans; Hyponatremia; Male; Pneumonia, Viral; Vasopressins; Water-Electrolyte Imbalance

Water depletion, water in excess and sodium depletion are the most important disturbance of sodium-water balance. Water, electrolytes and acid-base balance have always to be considered in their complex correlation because of their various interrdependency. The restoration of balance concerning imput and output is considered as a basic principle of any intravenous therapy.

Topics: Acid-Base Equilibrium; Extracellular Space; Humans; Infusions, Parenteral; Osmotic Pressure; Sodium; Vasopressins; Water Intoxication; Water Loss, Insensible; Water-Electrolyte Imbalance

Transient episodes of the syndrome of inappropriate anti-diuresis developped in two severe colchicine poisonings. These are the first cases reported. On patient also developped a reversible periphal neuropathy. The similarity of such accidents with vicristine neuro-toxicity is emphasized.

Topics: Adolescent; Alopecia; Bone Marrow Diseases; Diarrhea; Disseminated Intravascular Coagulation; Female; Humans; Hyponatremia; Psychomotor Disorders; Vasopressins; Water Intoxication; Water-Electrolyte Imbalance

A reversed diurnal excretory rhythm of water, creatinine and electrolytes was observed in a woman with fluid retention that first appeared following a head injury 21 years previously. Synthetic oxytocin injections were given on the premise that she had a selective deficiency of oxytocin with normal vasopressin production. This treatment produced a diuresis and restored a normal excretory rhythm of water, creatinine and electrolytes. Inulin and PAH clearance studies showed that oxytocin increased the daytime glomerular filtration rate. These results suggest the possibility that oxytocin has an additional non-obstetrical physiologic function, viz. the regulation of the normal diurnal rhythm of glomerular filtration rate.

Topics: Acid-Base Imbalance; Body Fluids; Circadian Rhythm; Diuresis; Diuretics; Electrolytes; Female; Glomerular Filtration Rate; Humans; Inulin; Kidney; Oxytocics; Oxytocin; Periodicity; Vasopressins; Water; Water-Electrolyte Balance; Water-Electrolyte Imbalance