pituitrin and Chronic-Disease

Modulating neurohormonal imbalance is the cornerstone of successful therapy in patients with chronic heart failure with reduced ejection fraction (HFrEF). Plasma arginine vasopressin (AVP) levels are elevated in HFrEF and may contribute to disease progression by excess signaling at either the V1a or V2 receptors. The effects of V1a receptor antagonism are almost completely unexplored, but V1a signaling is closely related to that for angiotensin II and blocking that receptor deserves further study. Interfering with V2 signaling causes free water diuresis and improves congestion without worsening renal function when added to loop diuretics but alone did not improve outcomes when carried into the post-acute phase in one large study. Outcomes in chronic HFrEF are quite good while outcomes in acute HF remain poor. Therefore, further study of V2 or combined V1/V2 blockade of the effects of AVP would most likely yield positive results in patients with acute HF, perhaps especially as alternative, not adjunctive therapy to loop diuretics.

Topics: Antidiuretic Hormone Receptor Antagonists; Chronic Disease; Disease Progression; Female; Heart Failure; Humans; Male; Neurophysins; Protein Precursors; Receptors, Vasopressin; Sodium Potassium Chloride Symporter Inhibitors; Stroke Volume; Vasopressins

Hyponatremia is a common water balance disorder that often poses a diagnostic or therapeutic challenge. Therefore, guidelines were developed by professional organizations, one from within the United States (2013) and one from within Europe (2014). This review discusses the diagnosis and treatment of hyponatremia, comparing the two guidelines and highlighting recent developments. Diagnostically, the initial step is to differentiate hypotonic from nonhypotonic hyponatremia. Hypotonic hyponatremia is further differentiated on the basis of urine osmolality, urine sodium level, and volume status. Recently identified parameters, including fractional uric acid excretion and plasma copeptin concentration, may further improve the diagnostic approach. The treatment for hyponatremia is chosen on the basis of duration and symptoms. For acute or severely symptomatic hyponatremia, both guidelines adopted the approach of giving a bolus of hypertonic saline. Although fluid restriction remains the first-line treatment for most forms of chronic hyponatremia, therapy to increase renal free water excretion is often necessary. Vasopressin receptor antagonists, urea, and loop diuretics serve this purpose, but received different recommendations in the two guidelines. Such discrepancies may relate to different interpretations of the limited evidence or differences in guideline methodology. Nevertheless, the development of guidelines has been important in advancing this evolving field.

Topics: Acute Disease; Algorithms; Chronic Disease; Diagnosis, Differential; Glycopeptides; Humans; Hyponatremia; Practice Guidelines as Topic; Vasopressins

Hypopituitarism refers to deficiency of one or more hormones produced by the anterior pituitary or released from the posterior pituitary. Hypopituitarism is associated with excess mortality, a key risk factor being cortisol deficiency due to adrenocorticotropic hormone (ACTH) deficiency. Onset can be acute or insidious, and the most common cause in adulthood is a pituitary adenoma, or treatment with pituitary surgery or radiotherapy. Hypopituitarism is diagnosed based on baseline blood sampling for thyroid stimulating hormone, gonadotropin, and prolactin deficiencies, whereas for ACTH, growth hormone, and antidiuretic hormone deficiency dynamic stimulation tests are usually needed. Repeated pituitary function assessment at regular intervals is needed for diagnosis of the predictable but slowly evolving forms of hypopituitarism. Replacement treatment exists in the form of thyroxine, hydrocortisone, sex steroids, growth hormone, and desmopressin. If onset is acute, cortisol deficiency should be replaced first. Modifications in replacement treatment are needed during the transition from paediatric to adult endocrine care, and during pregnancy.

Topics: Acute Disease; Adenoma; Adrenocorticotropic Hormone; Chronic Disease; Deamino Arginine Vasopressin; Gonadal Steroid Hormones; Gonadotropins, Pituitary; Hormone Replacement Therapy; Human Growth Hormone; Humans; Hydrocortisone; Hypophysectomy; Hypopituitarism; Pituitary Gland; Pituitary Hormones, Anterior; Pituitary Irradiation; Pituitary Neoplasms; Prolactin; Radiotherapy; Thyrotropin; Thyroxine; Vasopressins

Depression is a clinically heterogenous condition defined by sub-types that can have diametrically opposed features, such as sleep and appetite. Within the same individual these features may change over time, and different symptom clusters may respond selectively to different treatments. It has been hypothesized that different pathophysiological processes may be operating in the different sub-types of depression and specifically that Melancholic depression may be associated with relative overactivity, and Atypical depression with relative hypoactivity, of the hypothalamic drive of the HPA axis. A consistent finding that emerges from the literature is that the experience of depression alters over the course of the illness with the features of Atypical depression dominating a more chronic clinical picture. This suggests that different stress states characterize the different profiles of depression as the illness becomes more chronic. There is evidence that the corticotropin-releasing hormone (CRH) control of HPA axis output is reduced in Atypical, compared to Melancholic, sub-types, but there is no convincing evidence that overall HPA activity, i.e., cortisol output, reduces. We suggest that there is a "switch" in the regulation of the HPA system from CRH to arginine vasopressin (AVP) control as stress becomes more sustained or repeated; resulting in an altered homeostasis within the HPA system. Cortisol, and the neuropeptides CRH and AVP, have different neurobiological, behavioural and experiental effects. The "switch" process should result in different neuropeptide/cortisol combinations and ratios and may explain the changing profile of depression over time. The heuristic merit in making a distinction between the different clinical states of depression will be discussed.

Topics: Animals; Antidepressive Agents; Chronic Disease; Corticotropin-Releasing Hormone; Depression; Female; Humans; Hydrocortisone; Hypothalamo-Hypophyseal System; Male; Mice; Neurophysins; Pituitary-Adrenal System; Protein Precursors; Rats; Stress, Psychological; Vasopressins

Topics: Adrenomedullin; Chronic Disease; Endothelins; Heart Failure; Hemodynamics; Humans; Natriuretic Peptides; Renin-Angiotensin System; Sympathetic Nervous System; Vasopressins

Concomitant anemia, heart failure, and renal disease can be seen in a large proportion of patients with heart failure. The purpose of this review is to discuss the current definitions and mechanisms involved in this pathophysiological relationship, as well as the potential management and treatment options available for these patients.. Dysfunctional heart can promote the dysfunction of the kidneys through a variety of pathophysiological mechanism, the reciprocal holds true as well. Heart failure has been considered as the most common type of cardiovascular complication seen in patients with renal failure. Central to this relationship lies anemia, which can be the result or the cause of either heart or kidney disease.. Cardiorenal syndrome is a complex condition, which requires the collaboration and resources from cardiology, cardiac surgery, nephrology, and critical care. Of great importance is recognizing the presence of cardiorenal syndrome and appreciating the impact it can play on treatment options and survival.

Topics: Adenosine; Anemia; Chronic Disease; Diuretics; Heart Failure; Hemofiltration; Humans; Kidney Failure, Chronic; Prognosis; Renin-Angiotensin System; Risk Factors; Vasodilator Agents; Vasopressins

It is well established that endolymphatic hydrops plays a role in Ménière disease, even though the precise role is not fully understood and the presence of hydrops in the ear does not always result in symptoms of the disease. It nevertheless follows that a scientific understanding of how hydrops arises, how it affects the function of the ear, and how it can be manipulated or reversed could contribute to the development of effective treatments for the disease. Measurements in animal models in which endolymphatic hydrops has been induced have given numerous insights into the relationships between hydrops and other pathologic and electrophysiological changes, and how these changes influence the function of the ear. The prominent role of the endolymphatic sac in endolymph volume regulation, and the cascade of histopathological and electrophysiological changes that are associated with chronic endolymphatic hydrops, have now been established. An increasing number of models are now available that allow specific aspects of the interrelationships to be studied. The yclical nature of Ménière symptoms gives hope that treatments can be developed to maintain the ear in permanent state of remission, possibly by controlling endolymphatic hydrops, thereby avoiding the rogressive damage and secondary pathologic changes that may also contribute to the patient's symptoms.

Topics: Acute Disease; Aldosterone; Animals; Chronic Disease; Cyclic AMP; Disease Models, Animal; Endolymph; Endolymphatic Hydrops; Endolymphatic Sac; Hearing Loss; Humans; Intracranial Pressure; Ion Transport; Lipopolysaccharides; Magnetic Resonance Imaging; Noise; Vasopressins

Etiopathogenesis, diagnostics and therapy of hyponatremias are summarized for clinicians. Hyponatremia is the most common electrolyte abnormality. Mild to moderate hyponatremia and severe hyponatremia are found in 15-30% and 1-4% of hospitalized patients, respectively. Pathophysiologically, hyponatremias are classified into two groups: hyponatremia due to non-osmotic hypersecretion of vasopressin (hypovolemic, hypervolemic, euvolemic) and hyponatremia of non-hypervasopressinemic origin (pseudohyponatremia, water intoxication, cerebral salt wasting syndrome). Patients with mild hyponatremia are almost always asymptomatic. Severe hyponatremia is usually associated with central nervous system symptoms and can be life-threatening. Diagnostic evaluation of patients with hyponatremia is directed toward identifying the extracellular fluid volume status, the neurological symptoms and signs, the severity and duration of hyponatremia, the rate at which hyponatremia developed. The first step to determine the probable cause of hyponatremia is the differentiation of the hypervasopressinemic and non-hypervasopressinemic hyponatremias with measurement of plasma osmolality, glucose, lipids and proteins. For further differential diagnosis of hyponatremia, the determination of urine osmolality, the clinical assessment of extracellular fluid volume status and the measurement of urine sodium concentration provide important information. The most important representative of euvolemic hyponatremias is SIADH. The diagnosis of SIADH is based on the exclusion of other hyponatremic conditions; low plasma osmolality (<275 mosmol/kg) and inappropriate urine concentration (urine osmolality >100 mosmol/kg) are of pathognomic value. Acute (<48 hrs) severe hyponatremia (<120 mmol/l) necessitates emergency care with rapid restoration of normal osmotic milieu (1 mmol/l/hr increase rate of serum sodium). Patients with chronic symptomatic hyponatremia have a high risk of osmotic demyelination syndrome in brain if rapid correction of the plasma sodium occurs (maximal rate of correction of serum sodium should be 0.5 mmol/l/hr or less). The conventional treatments for chronic asymptomatic hyponatremia (except hypovolemic patients) include water restriction and/or the use of demeclocycline or lithium or furosemide and salt supplementation. Vasopressin receptor antagonists have opened a new forthcoming therapeutic era. V2 receptor antagonists, such as lixivaptan, tolvaptan, satavaptan and the V2+

Topics: Antidiuretic Hormone Receptor Antagonists; Azepines; Benzamides; Benzazepines; Blood Volume; Brain Diseases; Central Nervous System; Chronic Disease; Demeclocycline; Demyelinating Diseases; Diagnosis, Differential; Diuretics; Extracellular Fluid; Furosemide; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lithium Compounds; Morpholines; Osmolar Concentration; Osmosis; Pyrroles; Severity of Illness Index; Sodium; Spiro Compounds; Time Factors; Tolvaptan; Vasopressins

Vasopressin (VP) secreted from parvocellular neurons of the hypothalamic paraventricular nucleus (PVN) stimulates pituitary adrenocorticotropic hormone (ACTH) secretion, through interaction with receptors of the V1b subtype (V1bR) in the pituitary corticotroph, mainly by potentiating the stimulatory effects of corticotrophin-releasing hormone (CRH). Chronic stress paradigms associated with corticotroph hyperresponsiveness lead to preferential expression of hypothalamic VP over CRH and upregulation of pituitary V1bR, suggesting that VP has a primary role during adaptation of the hypothalamic pituitary adrenal (HPA) axis to long-term stimulation. However, studies using pharmacological or genetic ablation of V1bR have shown that VP is required for full ACTH responses to some stressors, but not for the sensitization of ACTH responses to a novel stress observed during chronic stress. Studies using minipump infusion of a peptide V1 antagonist in long-term adrenalectomized rats have revealed that VP mediates proliferative responses in the pituitary. Nevertheless, only a minor proportion of cells undergoing mitogenesis co-express markers for differentiated corticotrophs or precursors, suggesting that new corticotrophs are recruited from yet undifferentiated cells. The overall evidence supports a limited role of VP regulating acute ACTH responses to some acute stressors and points to cell proliferation and pituitary remodelling as alternative roles for the marked increases in parvocellular vasopressinergic activity during prolonged activation of the HPA axis.

Topics: Adrenocorticotropic Hormone; Anesthetics; Animals; Chronic Disease; Corticotropin-Releasing Hormone; Humans; Hypothalamo-Hypophyseal System; Paraventricular Hypothalamic Nucleus; Pituitary-Adrenal System; Receptors, Corticotropin; Receptors, Vasopressin; Rodentia; Stress, Psychological; Vasopressins

In chronic heart failure (CHF), persistent autonomic derangement and neurohumoral activation cause structural end-organ damage, decrease exercise capacity, and reduce quality of life. Beneficial effects of pharmacotherapy and of exercise training in CHF have been documented at various functional and structural levels. However, pharmacologic treatment can not yet reduce autonomic derangement and neurohumoral activation in CHF to a minimum. Various studies suggest that exercise training is effective in this respect.. After reviewing the available evidence we conclude that exercise training increases baroreflex sensitivity and heart rate variability, and reduces sympathetic outflow, plasma levels of catecholamines, angiotensin II, vasopressin, and brain natriuretic peptides at rest.. Exercise training has direct and reflex sympathoinhibitory beneficial effects in CHF. The mechanism by which exercise training normalizes autonomic derangement and neurohumoral activation is to elucidate for further development of CHF-related training programs aimed at maximizing efficacy while minimizing workload.

Topics: Arginine; Autonomic Nervous System Diseases; Baroreflex; Catecholamines; Chronic Disease; Endothelins; Exercise Therapy; Heart Failure; Heart Rate; Humans; Natriuretic Peptide, Brain; Neurotransmitter Agents; Renin-Angiotensin System; Treatment Outcome; Vasopressins

In a national heart failure registry, hyponatremia (serum sodium < 130 mEq/L) was initially reported in 5% of patients and considered a risk factor for increased morbidity and mortality. In a chronic heart failure study, serum sodium level on admission predicted an increased length of stay for cardiovascular causes and increased mortality within 60 days of discharge. Hyponatremia in patients with congestive heart failure (CHF) is associated with a higher mortality rate. Also, by monitoring and increasing serum sodium levels during hospitalization for CHF, patient outcomes may improve. This review describes the pathophysiology of hyponatremia in relation to CHF, including the mechanism of action of vasopressin receptors in the kidney, and assesses the preclinical and clinical trials of vasopressin receptor antagonists--agents recently developed to treat hyponatremia. In hospitalized patients with CHF, hyponatremia plays a major role in poor outcomes. Vasopressin receptor antagonists have been shown to be safe and effective in clinical trials in patients with hyponatremia.

Topics: Arginine Vasopressin; Azepines; Benzamides; Benzazepines; Chronic Disease; Clinical Trials as Topic; Diuretics; Heart Failure; Humans; Hyponatremia; Models, Biological; Pyrroles; Registries; Renin-Angiotensin System; Sodium; Tolvaptan; Treatment Outcome; Vasopressins

Topics: Arteriosclerosis; Catecholamines; Chronic Disease; Endothelium, Vascular; Heart Diseases; Humans; Inflammation; Kidney Diseases; Oxidative Stress; Renin-Angiotensin System; Risk Factors; Vasopressins

Critical illness is characterized by striking alterations in the hypothalamic-anterior-pituitary-peripheral-hormone axes, the severity of which is associated with a high risk of morbidity and mortality. Most attempts to correct hormone balance have been shown ineffective or even harmful because of a lack of pathophysiologic insight. There is a biphasic (neuro)endocrine response to critical illness. The acute phase is characterized by an actively secreting pituitary, but the concentrations of most peripheral effector hormones are low, partly due to the development of target-organ resistance. In contrast, in prolonged critical illness, uniform (predominantly hypothalamic) suppression of the (neuro)endocrine axes contributes to the low serum levels of the respective target-organ hormones. The adaptations in the acute phase are considered to be beneficial for short-term survival. In the chronic phase, however, the observed (neuro)endocrine alterations appear to contribute to the general wasting syndrome. With the exception of intensive insulin therapy, and perhaps hydrocortisone administration for a subgroup of patients, no hormonal intervention has proven to beneficially affect outcome. The combined administration of hypothalamic releasing factors does, however, hold promise as a safe therapy to reverse the (neuro)endocrine and metabolic abnormalities of prolonged critical illness by concomitant reactivation of the different anterior-pituitary axes.

Topics: Acute Disease; Adrenal Glands; Catecholamines; Chronic Disease; Critical Illness; Endocrine System; Gonads; Hormones; Models, Biological; Thyroid Gland; Vasopressins

Heart failure represents a major public health problem in the industrialized countries and despite of optimal medical treatment its mortality remains high. The history of its management reflects growth and changes in our understanding of its pathophysiology. In the past, pharmacological treatment of heart failure was aimed only at relieving edema and improving hemodynamics. Today, however, a major aim of treatment is to antagonize the sympathetic nervous system and renin-angiotensin-aldosterone system, to avert harmful effects of neurohormonal activation on the myocardium and peripheral vessels. Currently, the major pharmacological treatments for heart failure are diuretics, ACE inhibitors, beta-blockers and (in NYHA classes III-IV) aldosterone antagonists. Some patients may also require specific treatment with additional drugs (e.g. anti-arrhythmia agents, anticoagulants, or vasodilators) or procedures such as coronary revascularization, or implantable devices such as pacemakers and implantable cardioverter defibrillators, or resynchronization devices. Patients with end-stage heart failure may require cardiac transplantation or ventricular assist devices. This review is summarized the recent practical drug therapy of heart failure and the results of the newer clinical trial.

Topics: Adrenergic beta-Antagonists; Angiotensin II; Angiotensin-Converting Enzyme Inhibitors; Chronic Disease; Defibrillators, Implantable; Digitalis Glycosides; Diuretics; Endothelin Receptor Antagonists; Erythropoietin; Heart Failure; Heart-Assist Devices; Humans; Hungary; Immunologic Factors; Mineralocorticoid Receptor Antagonists; Pacemaker, Artificial; Peptide Hydrolases; Primary Prevention; Risk Factors; Severity of Illness Index; Vasopressins

Topics: Angiotensin-Converting Enzyme Inhibitors; Arginine; Chronic Disease; Diagnosis, Differential; Diuretics; Drug Therapy, Combination; Endothelin-1; Heart Failure; Humans; Hypertension; Prognosis; Renin-Angiotensin System; Vasopressins

Pathogenic mechanisms of chronic systolic heart failure are constantly of great interest. In recent years the neurohumoral theory of heart failure has gained attraction. According to this theory, neurohumoral mechanisms play the main role in the pathogenesis of heart failure, especially in its progression. These mechanisms can be divided into 2 categories: vasoconstrictive, mitogenic and antinatriuretic on the one hand and vasodilative, antimitogenic and natriuretic on the other one. The former consists of sympathetic nervous system, renin-angiotensin-aldosterone system, vasopressin, endothelin, cytokines. The latter comprises natriuretic peptides, prostaglandins and nitric oxide. Undoubtedly unfavourable roles of sympathetic system and renin-angiotensin-aldosteron have been shown in the progression of heart failure. Data are being also gathered confirming harmful effects of endothelin and cytokines and possibly of neuropeptide Y and vasopressine. Extensive data exist that demonstrate beneficial influence of natriuretic peptide on heart failure. The roles of nitric oxide as well as recently discovered adrenomedullin and medullipin are far from clear.

Topics: Chronic Disease; Cytokines; Disease Progression; Endothelin-1; Heart Failure; Humans; Natriuretic Agents; Neuropeptide Y; Nitric Oxide; Renin-Angiotensin System; Sympathetic Nervous System; Vasopressins

Topics: Catecholamines; Chronic Disease; Heart Failure; Hemodynamics; Humans; Myocardial Contraction; Renin-Angiotensin System; Vasopressins

Topics: Adrenocorticotropic Hormone; Brain; Calcifediol; Calcium; Chronic Disease; Estradiol; Estrogens; Female; Follicle Stimulating Hormone; Glucose; Growth Hormone; Hormones; Humans; Hypothalamo-Hypophyseal System; Hypothyroidism; Insulin; Liver Cirrhosis, Alcoholic; Liver Diseases; Luteinizing Hormone; Male; Melatonin; Neurotransmitter Agents; Parathyroid Hormone; Phosphorus; Pituitary Gland; Prolactin; Renin-Angiotensin System; Somatomedins; Testosterone; Thyroid Hormones; Thyrotropin-Releasing Hormone; Vasopressins; Vitamin D

Bleeding from esophageal varices is a feared complication of liver cirrhosis with high mortality. Pharmacotherapy of the acute bleeding episode with vasopressin has been shown to be effective in controlled studies, but side effects of this therapy are high and therefore replacement of vasopressin with somatostatin is under investigation. Another potential lead is the combination of vasopressin with vasodilators such as nitroglycerin. While acute pharmacotherapy of the patient with esophageal varices is well accepted, chronic or prophylactic pharmacotherapy is still in the investigative stage. Prophylactic therapy with beta-blockers, e.g. propranolol, has been shown to be effective in compensated patients with alcoholic cirrhosis. In patients with more advanced stages of the disease, or with cirrhosis of other etiology, the effectiveness of propranolol has not been proven. The mechanism of propranolol is similar to that of vasopressin, i.e. it lowers portal pressure by reducing portal flow. To maintain function of the affected organ, an alternative approach--namely lowering of portal pressure through reduction of the pathologically elevated resistance--should be actively investigated.

Topics: Acute Disease; Adrenergic beta-Antagonists; Chronic Disease; Clinical Trials as Topic; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Hypertension, Portal; Propranolol; Random Allocation; Somatostatin; Vasopressins

For 2 decades evidence accumulated that supported the Gauer-Henry hypothesis tying blood volume changes to the control of vasopressin (VP). By the mid 1970's this left atrial hypothesis was generally accepted even though there was a significant body of conflicting data and several definitive questions that had not been answered. In the last decade numerous investigations have addressed these questions and although there are better answers for some, others remain elusive. Pertinent work during the past 10 years is reviewed in the framework of some of these questions. The emphasis is placed on the location of the primary volume receptors, determination of the threshold for effects on VP, the degree of volume-pressure receptor and volume-osmotic receptor interactions, and species differences.

Topics: Animals; Aorta; Blood Volume; Chronic Disease; Dogs; Haplorhini; Heart Atria; Heart Failure; Humans; Osmotic Pressure; Pressoreceptors; Rats; Receptors, Angiotensin; Receptors, Cell Surface; Receptors, Vasopressin; Vasopressins

The genesis of renovascular hypertension follows a continuum from an acute to a chronic phase. Reduction in renal perfusion initiates renin release and angiotensin-mediated systemic vasoconstriction. Aldosterone secretion, sodium and water retention, and expansion of the extracellular volume ensue. Sustained hypertension is further maintained by interacting physiologic mechanisms including increased angiotensin II sensitivity, vasopressin, ouabain-like substance, the sympathetic nervous system, CNS mechanisms, autoregulation, and structural changes.

Topics: Acute Disease; Angiotensin II; Animals; Arterial Occlusive Diseases; Central Nervous System; Chronic Disease; Disease Models, Animal; Dogs; Hemodynamics; Hypertension, Renovascular; Kidney; Ouabain; Perfusion; Rats; Renin-Angiotensin System; Sympathetic Nervous System; Vasoconstriction; Vasopressins

In patients with chronic liver disease a dissociation of the two most important partial functions of the adrenal cortex may be observed. A widening of the zona glomerulosa is associated with an increased aldosterone secretion and an atrophy of the zona fasciculata with a decreased cortisol production rate. In acute alcoholic liver damage there are sometimes remarkable special features concerning the adrenal function. The pathogenesis of the altered C21-steroid hormone metabolism is nonuniform and depends upon the etiology of the liver disease. Following factors may play role: 1. Decreased activity of specific hepatic enzymes a)direct enzyme damage b)indirect enzyme activity decreasing processed by deficiency of hydrogen from NADPH 2. Decreased hepatic blood flow 3. Disturbance of intracellular transport of substrates (e.g. cholestasis 4. Changes of transport proteins. 5. Direct or reactive changes of other factors of hormonal feedback systems (hypothalamus-pituitary-adrenal or gonadal-system; renin-angiotensin-aldosterone-system).

Topics: Adrenal Cortex; Adrenocorticotropic Hormone; Aldosterone; Chronic Disease; Circadian Rhythm; Cortisone; Glucocorticoids; Humans; Hydrocortisone; Liver Diseases; Male; Metyrapone; Mineralocorticoids; Steroids; Vasopressins

Topics: Acute Disease; Arginine Vasopressin; Chronic Disease; Hyponatremia; Osmolar Concentration; Sodium Chloride; Urine; Vasopressins; Water; Water-Electrolyte Balance

The rate of acid excretion by the kidney appears to be determined by factors regulating the site and the rate of sodium reabsorption, rather than by a homeostatic mechanism that responds to systemic pH. This hypothesis, although unconventional, is supported by much experimental evidence, and it accounts for a wide variety of clinical and physiologic findings that heretofore have been difficult or impossible to explain.

Topics: Absorption; Acid-Base Imbalance; Acidosis; Alkalosis; Ammonia; Animals; Bicarbonates; Carbon Dioxide; Cations; Chronic Disease; Dogs; Homeostasis; Humans; Hydrogen-Ion Concentration; Hypercapnia; Kidney; Kidney Tubules; Minerals; Nephrons; Sodium; Vasopressins

Topics: Adrenocorticotropic Hormone; Animals; Blood Pressure; Chronic Disease; Disease Models, Animal; Epinephrine; Fatty Acids, Nonesterified; Female; Fetal Heart; Fetal Hypoxia; Glucagon; Glycogen; Heart Rate; Lactates; Norepinephrine; Pregnancy; Propranolol; Regional Blood Flow; Sheep; Vasopressins

Topics: Adenosine Triphosphate; Adenylyl Cyclases; Adrenocorticotropic Hormone; Animals; Chronic Disease; Cyclic AMP; Female; Follicle Stimulating Hormone; Glomerulonephritis; Humans; Kidney; Male; Menstruation; Phosphoric Diester Hydrolases; Pregnancy; Pyelonephritis; Rats; Sex Factors; Thyrotropin; Vasopressins

Topics: Aldosterone; Angiotensin II; Blood Pressure; Chronic Disease; Female; Humans; Hypertension, Renal; Kidney; Kidney Diseases; Norepinephrine; Placenta; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Pregnancy Complications, Cardiovascular; Renin; Time Factors; Vasopressins

Renal handling of sodium and water is abnormal in chronic kidney diseases. To study the function and regulation of the aquaporin-2 water channel (AQP2) and the epithelial sodium channel (ENaC) in autosomal dominant polycystic kidney disease (ADPKD), we measured urinary excretion of AQP2 (u-AQP2), the β-subunit of ENaC (u-ENaC(β)), cAMP (u-cAMP), and prostaglandin E(2) (u-PGE(2)); free water clearance (C(H2O)); fractional sodium excretion (FE(Na)); and plasma vasopressin (p-AVP), renin (p-Renin), angiotensin II (p-ANG II), aldosterone (p-Aldo), and atrial and brain natriuretic peptide (p-ANP, p-BNP) in patients with ADPKD and healthy controls during 24-h urine collection and after hypertonic saline infusion during high sodium intake (HS; 300 mmol sodium/day) and low sodium intake (LS; 30 mmol sodium/day). No difference in u-AQP2, u-ENaC(β), u-cAMP, u-PGE(2), C(H2O), and vasoactive hormones was found between patients and controls at baseline, but during HS the patients had higher FE(Na). The saline caused higher increases in FE(Na) in patients than controls during LS, but the changes in u-ENaC(β), p-Aldo, p-ANP, p-BNP, p-Renin, and p-ANG II were similar. Higher increases in u-AQP2 and p-AVP were seen in patients during both diets. In conclusion, u-AQP2 and u-ENaC(β) were comparable in patients with ADPKD and controls at baseline. In ADPKD, the larger increase in u-AQP2 and p-AVP in response to saline could reflect an abnormal water absorption in the distal nephron. During LS, the larger increase in FE(Na) in response to saline could reflect a defective renal sodium retaining capacity in ADPKD, unrelated to changes in u-ENaC(β).

Topics: Adolescent; Adult; Aged; Aldosterone; Angiotensin II; Aquaporin 2; Atrial Natriuretic Factor; Chronic Disease; Cross-Over Studies; Cyclic AMP; Dinoprostone; Epithelial Sodium Channels; Female; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Polycystic Kidney, Autosomal Dominant; Renin; Saline Solution, Hypertonic; Sodium; Vasopressins; Young Adult

The purpose of this study was to examine the renal effects of a V2 receptor arginine vasopressin (AVP) antagonist in heart failure.. Arginine vasopressin has been implicated in the renal water retention and dilutional hyponatremia associated with chronic heart failure.. We examined the effects of the oral, non-peptide, selective V2 receptor antagonist lixivaptan in 42 diuretic-requiring patients with mild-to-moderate heart failure in a randomized, double-blind, placebo-controlled, ascending single-dose study. After overnight fluid deprivation, patients received single-blind placebo on day -1 (baseline) and double-blind study medication (placebo [n = 12] or lixivaptan 10, 30, 75, 150, 250, or 400 mg [n = 5 per dose group]) on day 1, followed by 4 h of continued fluid restriction and additional 20 h with ad libitum fluid intake.. At all but the 10-mg dose, lixivaptan produced a significant and dose-related increase in urine volume over 4 h, compared with placebo. During 24 h, increases in urine volume ranged from 1.8 l with placebo to 3.9 l after the 400-mg lixivaptan dose (p < 0.01). These increases in urine volumes were accompanied by significant increases in solute-free water excretion. At higher doses, serum sodium was significantly increased; AVP antagonism was well tolerated in these patients.. These observations confirm a role for AVP in the renal water retention associated with heart failure and suggest that the V2 receptor antagonist lixivaptan may be a promising therapeutic agent for the treatment of heart failure.

Topics: Administration, Oral; Antidiuretic Hormone Receptor Antagonists; Cardiac Output, Low; Chronic Disease; Diuresis; Dose-Response Relationship, Drug; Double-Blind Method; Electrolytes; Female; Hormones; Humans; Male; Middle Aged; Osmolar Concentration; Severity of Illness Index; Sodium; Vasopressins

Dynamic changes of speech function were studied in patients with persistence aphatic disorders after stroke under the conditions of application of V2 vasopressin receptor agonist (1-desamino-8-D-arginin-vasopressin). A course of intranasal administration of the medical drug by using the double blind control showed a reliable reduction of frustration severity of expressive and impressive speech in patients with aphasias of different forms and degrees. A correlation of positive influence of vasopressin on speech, verbal memory and attention was found at efferent motor aphasias. The achieved effects preserved during a two-year catamnestic observation period. A repeated course of therapy resulted in an additional improvement of speech. Neuropeptide restored initially, in patients with aphasias, relatively simple forms of speech and later--complicated ones. This resulted in an improvement of speech functions which are regulated by both cerebral hemispheres. Supposedly, neuropeptide optimized the activity of both the right and left cerebral hemispheres. The stability of the obtained effects is explained by induction, due to vasopressin, of compensatory processes leading to reorganization of intercentral connections.

Topics: Administration, Intranasal; Aphasia; Brain; Chronic Disease; Hemostatics; Humans; Middle Aged; Receptors, Vasopressin; Vasopressins

In order to evaluate the activation of the sympathetic nervous and renin-angiotensin systems and antidiuretic hormone release in the setting of chronic liver disease, we studied 30 patients with cirrhosis who presented normal renal function. The cirrhotic patients were divided into two groups according to Child's score: 20 were Child A and 10 Child B. The control group consisted of 10 normal subjects. Blood samples were collected for determination of norepinephrine (NE), dopamine (DA), angiotensin I and II (AI and AII), and antidiuretic hormone (ADH), using the method of high-performance liquid chromatography (HPLC). No significant differences (p < 0.05) were found in the plasma levels of NE, DA, AI, and AII between the cirrhotic patients and the controls, although the absolute values observed in both groups of cirrhotics were clearly higher than in controls. The ADH levels were higher in Child B in comparison to Child A patients and controls, though this difference was not significant as well. Our results suggest a hormonal activation in cirrhotic patients, even in the early stages of hepatic disease (without ascites). We also noted an increase in ADH levels in Child B patients in relation to Child A and controls, although there was no difference in osmolality, suggesting a non-osmotic ADH release.

Topics: Adult; Angiotensin II; Chromatography, High Pressure Liquid; Chronic Disease; Dopamine; Hepatitis, Viral, Human; Humans; Liver Cirrhosis, Alcoholic; Liver Function Tests; Male; Middle Aged; Norepinephrine; Prognosis; Renin-Angiotensin System; Severity of Illness Index; Sympathetic Nervous System; Vasopressins

Bleeding from esophageal varices is a feared complication of liver cirrhosis with high mortality. Pharmacotherapy of the acute bleeding episode with vasopressin has been shown to be effective in controlled studies, but side effects of this therapy are high and therefore replacement of vasopressin with somatostatin is under investigation. Another potential lead is the combination of vasopressin with vasodilators such as nitroglycerin. While acute pharmacotherapy of the patient with esophageal varices is well accepted, chronic or prophylactic pharmacotherapy is still in the investigative stage. Prophylactic therapy with beta-blockers, e.g. propranolol, has been shown to be effective in compensated patients with alcoholic cirrhosis. In patients with more advanced stages of the disease, or with cirrhosis of other etiology, the effectiveness of propranolol has not been proven. The mechanism of propranolol is similar to that of vasopressin, i.e. it lowers portal pressure by reducing portal flow. To maintain function of the affected organ, an alternative approach--namely lowering of portal pressure through reduction of the pathologically elevated resistance--should be actively investigated.

Topics: Acute Disease; Adrenergic beta-Antagonists; Chronic Disease; Clinical Trials as Topic; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Hypertension, Portal; Propranolol; Random Allocation; Somatostatin; Vasopressins

A vasopressin derivative or placebo was administered to 21 chronic schizophrenia patients for 3 weeks in a randomized crossover double-blind design. The patients were divided into those above and below the median on baseline memory measured by the Wechsler memory scale. Vasopressin treatment did not improve memory either in those patients with below median baseline memory or in the group as a whole.

Topics: Adult; Chronic Disease; Clinical Trials as Topic; Deamino Arginine Vasopressin; Double-Blind Method; Female; Humans; Male; Memory Disorders; Middle Aged; Random Allocation; Schizophrenia; Vasopressins

Recently, chronic hyponatremia, even mild, has shown to be associated with poor quality of life and high mortality. The mechanism by which hyponatremia contributes to those symptoms, however, remains to be elucidated. Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a primary cause of hyponatremia. Appropriate animal models are crucial for investigating the pathophysiology of SIADH. A rat model of SIADH has been generally used and mouse models have been rarely used. In this study, we developed a mouse model of chronic SIADH in which stable and sustained hyponatremia occurred after 3-week continuous infusion of the vasopressin V2 receptor agonist 1-desamino-8-D-arginine vasopressin (dDAVP) and liquid diet feeding to produce chronic water loading. Weight gain in chronic SIADH mice at week 2 and 3 after starting dDAVP injection was similar to that of control mice, suggesting that the animals adapted to chronic hyponatremia and grew up normally. AQP2 expression in the kidney, which reflects the renal action of vasopressin, was decreased in dDAVP-infused water-loaded mice as compared with control mice that received the same dDAVP infusion but were fed pelleted chow. These results suggest that "vasopressin escape" occurred, which is an important process for limiting potentially fatal severe hyponatremia. Behavioral analyses using the contextual and cued fear conditioning test and T-maze test demonstrated cognitive impairment, especially working memory impairment, in chronic SIADH mice, which was partially restored after correcting hyponatremia. Our results suggest that vasopressin escape occurred in chronic SIADH mice and that chronic hyponatremia contributed to their memory impairment.

Topics: Animals; Behavior, Animal; Chronic Disease; Disease Models, Animal; Hyponatremia; Inappropriate ADH Syndrome; Male; Memory Disorders; Mice; Mice, Inbred C57BL; Vasopressins

Topics: Adolescent; Adult; Chronic Disease; Cognition Disorders; Female; Humans; Neuropsychological Tests; Oxytocin; Psychiatric Status Rating Scales; Schizophrenia; Schizophrenic Psychology; Vasopressins; Young Adult

The vasopressin- and oxytocin-degrading enzyme insulin-regulated aminopeptidase (IRAP) is expressed in various organs including the brain. However, knowledge about its presence in human hypothalamus is fragmentary. Functionally, for a number of reasons (genetic linkage, hydrolysis of oxytocin and vasopressin, its role as angiotensin IV receptor in learning and memory and others) IRAP might play a role in schizophrenia. We studied the regional and cellular localization of IRAP in normal human brain with special emphasis on the hypothalamus and determined numerical densities of IRAP-expressing cells in the paraventricular, supraoptic and suprachiasmatic nuclei in schizophrenia patients and controls. By using immunohistochemistry and Western blot analysis, IRAP was immunolocalized in postmortem human brains. Cell countings were performed to estimate numbers and numerical densities of IRAP immunoreactive hypothalamic neurons in schizophrenia patients and control cases. Shape, size and regional distribution of IRAP-expressing cells, as well the lack of co-localization with the glia marker glutamine synthetase, show that IRAP is expressed in neurons. IRAP immunoreactive cells were observed in the hippocampal formation, cerebral cortex, thalamus, amygdala and, abundantly, hypothalamus. Double labeling experiments (IRAP and oxytocin/neurophysin 1, IRAP with vasopressin/neurophysin 2) revealed that IRAP is present in oxytocinergic and in vasopressinergic neurons. In schizophrenia patients, the numerical density of IRAP-expressing neurons in the paraventricular and the suprachiasmatic nuclei is significantly reduced, which might be associated with the reduction in neurophysin-containing neurons in these nuclei in schizophrenia. The pathophysiological role of lowered hypothalamic IRAP expression in schizophrenia remains to be established.

Topics: Aged; Autopsy; Chronic Disease; Cystinyl Aminopeptidase; Female; Glutamate-Ammonia Ligase; Humans; Hypothalamus; Male; Middle Aged; Neurons; Neurophysins; Oxytocin; Paraventricular Hypothalamic Nucleus; Pituitary Gland, Posterior; Schizophrenia; Suprachiasmatic Nucleus; Vasopressins

Parent-offspring interactions early in life can permanently shape the developmental path of those offspring. Manipulation of maternal care has long been used to alter the early-life environment of infants and impacts their later social behavior, aggression, and physiology. More recently, naturally occurring variation in maternal licking and grooming behavior has been shown to result in differences in social behavior and stress physiology in adult offspring. We have developed a model of natural variation in biparental care in the prairie vole (Microtus ochrogaster) and have demonstrated an association between the amount of early care received and later social behavior. In this study, we investigate the relationship between early life care and later aggression and neuroendocrine responses following chronic social isolation. Male and female offspring were reared by their high-contact (HC) or low-contact (LC) parents, then housed for 4 weeks post-weaning in social isolation. After 4 weeks, half of these offspring underwent an intrasexual aggression test. Brains and plasma were collected to measure corticotropin-releasing hormone (CRH) and vasopressin (AVP) immunoreactivity and plasma corticosterone (CORT). Male offspring of LC parents engaged in more aggressive behavior in the intrasexual aggression test compared to HC males. Female offspring of HC parents had higher plasma CORT levels after chronic social isolation and increases in the number and density of AVP-immunopositive cells in the supraoptic nucleus following an intrasexual aggression test. These findings show that the impact of early life biparental care on behavior and HPA activity following a social stressor is both sex-dependent and early experience-specific.

Topics: Aggression; Animals; Arvicolinae; Body Weight; Chronic Disease; Corticosterone; Corticotropin-Releasing Hormone; Female; Male; Maternal Behavior; Paternal Behavior; Random Allocation; Sex Characteristics; Social Isolation; Stress, Psychological; Supraoptic Nucleus; Vasopressins

A co-morbidity of sleep-disordered breathing is hypertension associated with elevated sympathetic nerve activity, which may result from chronic intermittent hypoxia (CIH). CIH evokes plasticity in cardiorespiratory regulating sites, including the paraventricular nucleus (PVN), which acts to sustain increased sympathetic nerve activity. Our working hypothesis is that vasopressin neurons mediate the sustained increase in blood pressure and altered breathing associated with CIH. In a series of neuroanatomical experiments, we determined if vasopressin-containing PVN neurons innervate rostral ventrolateral medulla (RVLM), and altered cardiorespiratory responses induced by CIH conditioning (8h/day for 10 days) is mediated by vasopressin-V(1A ) receptor signaling in the medulla. In the first set of experiments, cholera toxin β subunit was microinjected into the RVLM to delineate innervation of the PVN. Immunohistochemistry data showed vasopressin-containing PVN neurons were double-labeled with cholera toxin β subunit, indicating vasopressin projection to the RVLM. In the second set, sections of the medulla were immunolabeled for vasopressin V(1A ) receptor, and its expression was significantly higher in the RVLM and in the neighboring rostral ventral respiratory column in CIH- than from RA-conditioned rats. In a series of physiological experiments,we determined if blocking the vasopressin V(1A )receptor in the medulla would normalize blood pressure in CIH-conditioned rats and also attenuate the evoked responses to PVN disinhibition.Blood pressure, heart rate, diaphragmatic and genioglossus muscle activity were recorded in anesthetized, ventilated and vagotomized rats. The PVN was disinhibited by microinjecting bicuculline before and after blocking vasopressin V(1A ) receptors in the RVLM/rostral ventral respiratory column. In RA-conditioned rats, PVN disinhibition increased blood pressure, heart rate, minute diaphragmatic and genioglossus muscle activity, and these increases were attenuated after blocking the vasopressin V(1A ) receptor. In CIH-conditioned rats, a significantly greater dose of blocker was required to blunt these physiological responses and it also normalized the baseline blood pressure. Our findings indicate that vasopressin is the neuropeptide released from PVN neurons that modulates cardiorespiratory output via the RVLM and rostral ventral respiratory column.

Topics: Animals; Bicuculline; Blood Pressure; Chronic Disease; Diaphragm; GABA-A Receptor Antagonists; Heart Rate; Hypertension; Hypoxia; Medulla Oblongata; Neurons; Paraventricular Hypothalamic Nucleus; Rats; Rats, Sprague-Dawley; Receptors, Vasopressin; Signal Transduction; Sleep Apnea Syndromes; Vasopressins

The hypothalamic nonapeptide vasopressin is a known player in the pathogenesis of chronic heart failure. According to the large body of clinical evidence, vasopressin has an impact on salt and water imbalance, hyponatremia, and subsequent renal insufficiency - the most common and destructive co-morbidity of patients afflicted with chronic heart failure. Despite the well-documented elevated levels of vasopressin in the blood of such patients, its expression in the magnocellular hypothalamic nuclei and transport to the posterior pituitary has not yet been investigated. In addition, the literature almost lacks the information on the contribution of another member of nonapeptide family, oxytocin, in the pathogenesis of this disease. Here we present a postmortem analysis of vasopressin and oxytocin-immunoreactive neurons and their terminals in the posterior pituitary of 8 male patients (53.8+/-9.3 years) who had died from CHF and 9 male controls (54.6+/-11.8 years). In line with previous clinical reports, our study on hypothalami of chronic heart failure patients revealed a significant increase in the relative profile density (+29%) of vasopressin-positive neurons in the hypothalamic supraoptic nucleus. Consistently we found a significant increase in the relative optic density of vasopressin-immunoreactivity in the posterior pituitary (+33%) of these patients. In contrast, the similar analysis applied for oxytocin neurons revealed no statistically significant differences to controls. In conclusion, our study provides the morphological evidence for activation of vasopressin (but not oxytocin) expression and vasopressin transport to the posterior pituitary in patients with chronic heart failure.

Topics: Cadaver; Chronic Disease; Gene Expression; Heart Failure; Humans; Hypothalamo-Hypophyseal System; Male; Middle Aged; Oxytocin; Vasopressins

Topics: Antidiuretic Hormone Receptor Antagonists; Benzazepines; Chronic Disease; Heart Failure; Humans; Hyponatremia; Sodium; Tolvaptan; Vasopressins

Many psychiatric disorders are a result of a disturbance in or exhaustion of the human stress response system. It is striking that many of these disorders such as depression, anxiety disorders and post-traumatic stress and somatoform and dissociative disorders are more prevalent in women. There are various explanations for this differing prevalence: it can be attributed to molecular, genetic, neurophysiological, relational and neurohormonal differences. Among the topics discussed are differences in exposure to chronic and traumatic stressors, the role of vasopressin and oxytocin in recovery and neurophysiological differences, the differentiating effect of hormones and neuropeptides such as oxytocin and vasopressin, the tend and befriend response and factors such as abuse and attachment disruption in early childhood.

Topics: Anxiety Disorders; Chronic Disease; Depressive Disorder; Dissociative Disorders; Female; Genetic Predisposition to Disease; Humans; Male; Oxytocin; Prevalence; Sex Factors; Stress Disorders, Post-Traumatic; Stress, Psychological; Vasopressins

In males, long-term alcohol consumption provokes neurochemical changes in the medial parvocellular division of the PVN (PVNmp) that are partially reversed by withdrawal. Because gonadal steroids modulate the activity of the hypothalamo-pituitary-adrenal axis, we analyzed the possibility that the repercussions of chronic alcohol consumption and withdrawal on the anatomy and neurochemistry of the PVNmp might differ between the sexes. Male and female Wistar rats were examined after ingesting a 20% alcohol solution for 6 months or after 2 months of withdrawal from 6 months of alcohol consumption. The levels of gonadal steroids and the basal concentrations of corticosterone were also evaluated. Chronic alcohol consumption and withdrawal did not alter the global cytoarchitectonic features of the PVNmp in rats of both sexes. However, alcohol consumption was associated with a decrease in the number of vasopressin (VP) neurons only in females and of corticotropin releasing hormone (CRH) neurons in males and females. Further, the response to withdrawal was sexually dimorphic because in males there was a partial recovery of the number of CRH neurons whereas in females there was a further loss of VP and CRH neurons. Corticosterone levels were unchanged by alcohol consumption, but they were decreased by withdrawal in females. Alcohol consumption and withdrawal did not alter estrogen and progesterone concentrations in females, but decreased testosterone levels in males. These findings show that the response of CRH and VP neurons to excess alcohol is gender-specific, with females being more vulnerable during alcohol consumption and, most notably, after withdrawal.

Topics: Alcohol-Induced Disorders, Nervous System; Alcoholism; Animals; Cell Death; Chronic Disease; Corticosterone; Corticotropin-Releasing Hormone; Disease Models, Animal; Down-Regulation; Female; Gonadal Steroid Hormones; Gonads; Hypothalamo-Hypophyseal System; Male; Nerve Degeneration; Paraventricular Hypothalamic Nucleus; Pituitary-Adrenal System; Rats; Rats, Wistar; Sex Characteristics; Substance Withdrawal Syndrome; Vasopressins

Previous studies have demonstrated that type 1 diabetes is characterized by hypercorticism and lack of periodicity in adrenal hormone secretion. In the present study, we tested the hypothesis that hypercorticism is initiated by an enhanced release of ACTH leading subsequently to adrenocortical growth and increased output of adrenocortical hormones. To test this hypothesis, we used the streptozotocin (STZ)-induced diabetes mouse model and measured hypothalamic-pituitary-adrenal axis activity at different time points. The results showed that the expected rise in blood glucose levels induced by STZ treatment preceded the surge in corticosterone secretion, which took place 1 d after diabetes onset. Surprisingly, circulating ACTH levels were not increased and even below control levels until 1 d after diabetes onset and remained low until d 11 during hypercorticism. In response to ACTH (but not vasopressin), cultures of adrenal gland cells from 11-d diabetic mice secreted higher amounts of corticosterone than control cells. Real-time quantitative PCR revealed increased expression of melanocortin 2 and melanocortin 5 receptors in the adrenal glands at 2 and 11 d of STZ-induced diabetes. AVP mRNA expression in the paraventricular nucleus of the hypothalamus was increased, whereas hippocampal MR mRNA was decreased in 11-d diabetic animals. GR and CRH mRNAs remained unchanged in hippocampus and paraventricular nucleus of diabetic mice at all time points studied. These results suggest that sensitization of the adrenal glands to ACTH rather than an increase in circulating ACTH level is the primary event leading to hypercorticism in the STZ-induced diabetes mouse model.

Topics: Adrenal Glands; Adrenocortical Hyperfunction; Adrenocorticotropic Hormone; Animals; Blood Glucose; Body Weight; Cells, Cultured; Chronic Disease; Corticosterone; Corticotropin-Releasing Hormone; Diabetes Mellitus, Experimental; Hypothalamo-Hypophyseal System; In Situ Hybridization; Male; Mice; Organ Size; Pituitary-Adrenal System; Radioimmunoassay; Receptor, Melanocortin, Type 2; Receptors, Corticotropin; Receptors, Melanocortin; Receptors, Mineralocorticoid; Reverse Transcriptase Polymerase Chain Reaction; Time Factors; Vasopressins

Vasopressin plays an important role in the hypothalamo-pituitary-adrenal axis regulation as well as in stress-related disorders. A common view suggested that the role of vasopressin is especially important during chronic stresses. Here we tested the hypothesis that vasopressin-deficient rats may be more resistant to the development of chronic hypothalamo-pituitary-adrenal axis hyperactivity after chronic mild stress.. Male vasopressin deficient Brattleboro rats were compared to their heterozygous litter mates. Chronic mild stress consisted of different mild stimuli (e.g. wet cages, restraint) for 6 week. The corticosterone changes were followed by repeated tail cutting and organs and blood were collected from decapitated rats.. In controls, chronic mild stress resulted in symptoms of chronic stress state characterized by typical somatic (body weight reduction, thymus involution) and endocrine changes (resting plasma ACTH and corticosterone elevation and POMC mRNA elevation in anterior lobe of the pituitary). Unexpectedly, the lack of vasopressin could not influence any chronic mild stress-induced changes.. Somatic changes and endocrine effects of chronic mild stress are similar in control and vasopressin deficient animals. This suggests that either vasopressin is not indispensable for activating the hypothalamo-pituitary-adrenal axis by chronic stress or the absence of vasopressin is compensated by other mediators (e.g. CRH) in Brattleboro rats.

Topics: Adrenal Glands; Adrenocorticotropic Hormone; Animals; Body Weight; Chronic Disease; Corticosterone; Depression; Disease Models, Animal; Heterozygote; Hypothalamo-Hypophyseal System; Male; Organ Size; Pituitary Gland, Anterior; Pituitary-Adrenal System; Pro-Opiomelanocortin; Rats; Rats, Brattleboro; Stress, Psychological; Thymus Gland; Vasopressins

A 71-year old man with failed back syndrome was admitted to hospital with oliguria that had occurred 4 days after his dose of paroxetine had been increased to 40 mg x day(-1). Laboratory data on admission revealed hyponatremia (124 mmol x l(-1)), low serum osmolarity (267 mOsm x l(-1)) with a normal level of serum antidiuretic hormone (1.7 pg x ml(-1)), and concentrated urine (430 mOsm x l(-1)). He was diagnosed as having syndrome of inappropriate secretion of antidiuretic hormone, associated with paroxetine; this drug was discontinued immediately after admission. The hyponatremia was treated with saline infusion, water restriction, and furosemide; serum sodium level returned to normal on hospital day 5. Paroxetine is being increasingly used for depression and chronic pain management because of its favorable side-effect profile; however, we should be alert to hyponatremia in patients on paroxetine by carrying out periodic monitoring of serum electrolytes, especially in elderly patients.

Topics: Aged; Antidepressive Agents, Second-Generation; Chronic Disease; Depressive Disorder; Electrolytes; Humans; Hyponatremia; Inappropriate ADH Syndrome; Intervertebral Disc Displacement; Male; Pain; Paroxetine; Sodium; Spinal Stenosis; Vasopressins

Although acute decreases in plasma volume are known to enhance the osmotically induced arginine vasopressin (AVP) release, it is unclear whether there is also such interaction at the level of gene transcription. It also remains to be established how sustained changes in plasma volume affect the osmoregulation. In this study, we examined how acute and chronic decreases in blood volume affected the osmoregulation of AVP release and gene transcription in rats. Acute hypovolemia was induced by intraperitoneal injection of polyethylene glycol (PEG), and chronic hypovolemia was induced by 3 days of water deprivation (WD) or 12 days of salt loading (SL). Rats were injected with isotonic or hypertonic saline, and plasma AVP levels and AVP heteronuclear (hn)RNA expression in the supraoptic and paraventricular nuclei, an indicator of gene transcription, were examined in relation to plasma osmolality in each group. Plasma AVP levels were correlated with plasma Na levels in all groups. Whereas the regression lines relating plasma AVP to Na were almost identical among control, WD, and SL groups, the thresholds of plasma Na for AVP release were significantly decreased only in the PEG group. AVP hnRNA levels were also correlated with plasma Na levels in control and PEG groups, and the thresholds were significantly decreased in the PEG group. In contrast, there was no significant correlation of AVP hnRNA and plasma Na levels in WD and SL groups. Thus it was demonstrated that acute and chronic reduction in plasma volume affected the osmoregulation of AVP release and gene transcription in different ways.

Topics: Acute Disease; Animals; Blood Proteins; Chronic Disease; Gene Expression Regulation; Hypovolemia; Male; Plasma Volume; Polyethylene Glycols; Rats; Rats, Sprague-Dawley; Sodium; Transcription, Genetic; Vasopressins; Water-Electrolyte Balance

The hyperosmolality associated with diabetes mellitus triggers an increase in neuronal activity and vasopressin production within magnocellular neurosecretory cells (MNCs) of the hypothalamic supraoptic nucleus (SON). In this study, we examined the effect of chronic diabetes on the function and survival of these neurons. After 6 months, but not 6 weeks, of streptozotocin (STZ)-induced diabetes, we observed an increase in the appearance of small hyperchromatic neurons and a decrease in SON neuronal density. A subpopulation of neurons within the SON at this time point demonstrated positive staining for cleaved caspase-3 and TUNEL, two markers of apoptosis. In addition, the number of vasopressin-positive neurons was decreased. Markers for apoptosis did not colocalize with vasopressin immunopositivity; this was probably due to a diabetes-induced degenerative process causing downregulation of vasopressin expression or depletion of neuropeptide. Although the phenotypes of the apoptotic neurons were not identified, other SON neurons including oxytocin-producing neurons are unlikely to be affected by chronic hyperglycemia. Microglial hypertrophy and condensation were also observed in the 6-month diabetic SON. Although upregulation of vasopressin production in response to acute hyperosmolality is adaptive, prolonged overstimulation of vasopressin-producing neurons in chronic diabetes results in neurodegeneration and apoptosis.

Topics: Animals; Antigens, CD; Antigens, Neoplasm; Antigens, Surface; Apoptosis; Avian Proteins; Basigin; Blood Proteins; Caspase 3; Caspases; Chronic Disease; Diabetes Mellitus, Experimental; Disease Models, Animal; Down-Regulation; Glial Fibrillary Acidic Protein; Gliosis; In Situ Nick-End Labeling; Male; Membrane Glycoproteins; Microglia; Nerve Degeneration; Neurons; Rats; Rats, Sprague-Dawley; Supraoptic Nucleus; Vasopressins; Water-Electrolyte Balance

Clinical results of the Maze procedure for treatment of atrial fibrillation (AF) are excellent, suggesting improved ventricular function after restoring sinus rhythm. However, long-term corresponding effects on the release of cardiac natriuretic peptides and other vasoactive hormones are incompletely investigated after isolated Maze surgery.. Plasma levels of brain natriuretic peptide (BNP), atrial natriuretic peptide (ANP), antidiuretic hormone, aldosterone, and angiotensin II were measured in 15 patients (mean age, 52 +/- 11 years) undergoing isolated surgical Maze (III) procedures for medically refractory AF, preoperatively and 6 months postoperatively. At the time of blood sampling, hemodynamic correlates were obtained at baseline and after 6 and 12 minutes of rapid ventricular pacing at 150 stimulations/minute.. All patients were free of AF at 6-month follow-up. The measured plasma levels of BNP, ANP, and angiotensin II were all significantly lower (p = 0.03) late after the isolated Maze procedure. Cardiac output was significantly higher postoperatively (p < 0.01). Other hemodynamic values and left atrial size were unchanged after surgery. Ventricular pacing caused almost identical hemodynamic changes in atrial pressures before and late after surgery, but the associated plasma ANP response was significantly attenuated postoperatively (p < 0.001).. Levels of cardiac natriuretic peptides and angiotensin II as markers of ventricular function are improved in the long term after clinically successful isolated Maze procedures. ANP response to hemodynamic challenge by ventricular pacing was attenuated postoperatively, possibly due to atrial scarring.

Topics: Adult; Aged; Aldosterone; Angiotensin II; Atrial Fibrillation; Atrial Natriuretic Factor; Chronic Disease; Cryosurgery; Female; Follow-Up Studies; Hemodynamics; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Neurotransmitter Agents; Postoperative Complications; Vasopressins; Ventricular Dysfunction, Left; Ventricular Function, Left

Septic shock is still the major cause of death in surgical intensive care unit. Fluid support, inotropic agents, and broad spectrum antibiotics are still the mainstay of traditional therapy. Here, we present a case of septic shock arising from gangrenous ischemic bowel, complicated by chronic pulmonary hypertension, which was refractory to catecholamine vasoprerssors. We successfully stabilized the hemodynamics and reduce the pulmonary hypertension with low-dose vasopressin infusion.

Topics: Aged; Chronic Disease; Female; Humans; Hypertension, Pulmonary; Infusions, Intravenous; Shock, Septic; Vasoconstrictor Agents; Vasopressins

The aim of this study was to develop a new model of vasopressin-induced chronic myocardial damage based on sustained ST-segment depression in electrocardiogram (ECG) with progression of myocardial fibrosis in rats. Furthermore, using this model, we examined the prophylactic potential of fasudil, a Rho-kinase inhibitor, against myocardial damage induced by vasopressin. In 10-week old male Donryu rats, intravenous administration of arginine vasopressin (0.5 iu/kg) induced significant ST-segment depression. Two days and one week after the administration of vasopressin, ST-segment depression was -0.19 +/- 0.02 and -0.14 +/- 0.02 mV, respectively. Fasudil (10 and 30 mg/kg, p.o.) significantly attenuated the ST-segment depression induced by vasopressin. One week after the administration of vasopressin, the percent area of myocardial fibrosis in control animals (0.42 +/- 0.11%, p < 0.01) was significantly greater than that in normal animals (0.05 +/- 0.01%). Fasudil (10 and 30 mg/kg) significantly prevented the development of the fibrosis. We present a new model of chronic myocardial damage based on sustained ST-segment depression with progression of myocardial fibrosis in rats, and suggest that this model may be useful to investigate the treatment of chronic angina. Inhibition of Rho-kinase is efficacious in preventing the ECG change and development of fibrosis induced by vasopressin in this model.

Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Animals; Cardiomyopathies; Chronic Disease; Disease Models, Animal; Disease Progression; Electrocardiography; Enzyme Inhibitors; Fibrosis; Intracellular Signaling Peptides and Proteins; Kinetics; Male; Protein Serine-Threonine Kinases; Rats; rho-Associated Kinases; Vasopressins

Acute myocardial infarction evokes activation of, among others, the arginine-vasopressin system, resulting in vasoconstriction and fluid retention. In the present study, the vasoconstrictor and antidiuretic effects of vasopressin were examined in vivo in conscious rats with chronic myocardial infarction, in the absence or presence of the V(1a) receptor antagonist SR-49059 or the V(2) receptor antagonist OPC-31260. In sham rats, vasopressin dose-dependently increased mean arterial pressure (maximum response: 45+/-3 mm Hg), which was significantly suppressed in infarcted rats (maximum response: 32+/-3 mm Hg). SR-49059, but not OPC-31260, caused a significant rightward shift of the dose pressure response curve in sham rats, indicating V(1a) receptor mediation. This rightward shift by SR-49059 was significantly more in infarcted rats. The suppressed response to the agonist and enhanced sensitivity to the antagonist suggest a reduction of V(1a) receptor number in infarcted rats. In both sham and infarcted rats, the urine production after OPC-31260 (337+/-14 and 329+/-30 microl/min, respectively) was about twice of that in vehicle-treated rats (188+/-25 and 155+/-24 microl/min, respectively). However, the response in infarcted rats reached its peak quicker and lasted for a shorter period, resulting in a 40% lower area under the curve. Although only measurable during V(2) receptor blockade, the reduction of urine production by vasopressin was significantly more in infarcted compared to sham rats. The enhanced renal response to the agonist and reduced response to the antagonist suggest an increase in V(2) receptor number in infarcted rats. In conclusion, in chronically infarcted rats, vasopressin causes vasoconstriction and fluid retention through the V(1a) and V(2) receptors, respectively. Altered responses after infarction indicate a shift from V(1a) to V(2) receptors.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Blood Pressure; Chronic Disease; Consciousness; Coronary Vessels; Dose-Response Relationship, Drug; Indoles; Kidney; Ligation; Male; Myocardial Infarction; Pyrrolidines; Rats; Rats, Wistar; Receptors, Vasopressin; Urination; Urodynamics; Vasopressins

Topics: Acute Disease; Aquaporins; Brain Edema; Chronic Disease; Humans; Hyponatremia; Hypovolemia; Vasopressins; 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

Previous short-term studies demonstrated that treatment with clonidine produced significant hemodynamic improvement in patients with congestive heart failure (CHF). In this study we followed 12 CHF patients (10 M, 2 F age 63+/-11, 10 with ischemic cardiomyopathy and 2 with dilated cardiomyopathy) treated with 0.15 or 0.075 mg oral clonidine twice daily for 13+/-5 months (range 6-23). with functional evaluation at baseline, 6 weeks and 6 months. There was suppression of circulating catecholamines, associated with significant ameliorations in NYHA class, in duration of exercise tolerance (from 246+/-68 sec to 362+/-30 and 459+/-70 sec, respectively p < 0.02), in ejection fraction (from 32+/-7% to 35+/-5 and 39+/-7% p < 0.04) and in left ventricular enlargement as assessed echocardiographically. There were also improvements in a number of electrophysiologic parameters calculated by computerized analysis of ambulatory ECG tapes, such as heart rate variability, indicating diminished propensity to malignant arrhythmias, as confirmed by decreases in the numbers of isolated premature ventricular contractions, couplets and episodes of non-sustained ventricular tachycardia. The data suggest that chronic central sympathetic suppression with clonidine in CHF results in significant functional amelioration and improved electrophysiologic stability.

Topics: Administration, Oral; Catecholamines; Chronic Disease; Clonidine; Echocardiography; Electrocardiography, Ambulatory; Exercise Test; Female; Heart Failure; Heart Rate; Humans; Male; Middle Aged; Neural Inhibition; Prospective Studies; Renin; Sympathetic Nervous System; Sympatholytics; Vasopressins

Neurohormonal activation and elevated ventricular filling pressures are prominent features in heart failure. Carmoxirole is a DA2 receptor agonist with limited central activity that modulates sympathetic activation and subsequently reduces pre-load and afterload in animals. The effect of carmoxirole on neurohormones and hemodynamics in humans was evaluated in 12 normotensive patients with NYHA class III-IV heart failure on stable ACE 1 and diuretic therapy. Carmoxirole (0.25-1.00 mg) was administered on 2 consecutive days, and hemodynamic and neurohormonal measurements were carried out. Values given are maximal percent changes from prestudy baseline (significance level P < 0.05). The lower dose on day 1 (0.25-0.50 mg) reduced circulating norepinephrine, vasopressin, and ANP by 40%, 19%, and 25%, respectively. In addition, on day 2, at a dose level of 0.75-1.00 mg, plasma renin activity decreased by 30%. Mean arterial pressure and systemic vascular resistance were reduced by 10% and 18%, and pulmonary wedge and right atrial pressure by 38% and 39%, respectively. Cardiac index improved by 20%. Despite a concomitant 12% reduction in heart rate, both stroke volume and stroke work index increased by 32% and 31%, respectively. Mean pulmonary artery pressure decreased by 21%, whereas pulmonary resistance was not affected. Thus, carmoxirole modulates sympathetic activation, accompanied by changes in vasopressin and ANP, and the renin-angiotensin system at higher dosages. These effects lead to a reduction in systemic resistance and heart rate, and an improvement in cardiac pump function and left and right ventricular filling pressures. It is concluded that carmoxirole induces beneficial effects on hemodynamic and neurohumoral parameters in heart failure.

Topics: Aged; Atrial Natriuretic Factor; Blood Pressure; Cardiac Output; Chronic Disease; Dopamine Agonists; Electrocardiography; Female; Heart Failure; Heart Rate; Humans; Indoles; Male; Neurotransmitter Agents; Norepinephrine; Pulmonary Wedge Pressure; Pyridines; Receptors, Dopamine D2; Vasopressins

The neurochemical and behavioural effects of a novel stereotaxic surgical method developed for interrupting the nerve fibres running through the rat pituitary stalk to the posterior pituitary gland was studied. The cerebrospinal fluid (CSF) vasopressin (AVP) and oxytocin (OT) content as well as changes in aggressiveness were measured in rats one week and one month after the surgical intervention. The main results are as follows: (1) the compression of the pituitary stalk elicits a chronic increase in water consumption, as well as in CSF vasopressin and oxytocin content; (2) the surgical intervention increased the frequency of clinch fighting after one week. The increase in aggressiveness accentuated after one month and, in addition, operated animals showed reduced scores of resting while exploratory and social behaviours increased; (3) there was a strong positive correlation between water consumption, vasopressin, and aggressiveness; (4) oxytocin changes showed a positive correlation with variation in social behaviour. The surgical intervention may serve as a model for lesions of the pituitary stalk and formation of ectopic neurohypophyses in humans.

Topics: Aggression; Animals; Behavior, Animal; Chronic Disease; Diabetes Insipidus; Drinking; Male; Nerve Compression Syndromes; Oxytocin; Pituitary Gland; Rats; Rats, Wistar; Social Behavior; Vasopressins

We investigated the relationship between exercise capacity and the level of neurohormonal activation at rest and during exercise in patients with various degrees of severity of chronic heart failure. We performed exercise testing with measurements of peak oxygen consumption (pVo2) and blood sampling at rest and at peak exercise in eight patients with moderate heart failure (pVo2 = 17 +/- 0.4 ml/kg/min) (mean +/- S.E.M.) and eight patients with severe CHF (pVo2 = 9 +/- 1 ml/kg/min). None of the patients was taking angiotensin converting enzyme inhibitors or beta-blockers. Plasma levels of atrial natriuretic peptide, cGMP, arginine-vasopressin, renin, angiotensin II, epinephrine and norepinephrine increased significantly (P < 0.01), from rest to peak exercise, in all patients. Among all the studied neurohormonal factors, only atrial natriuretic peptide levels at rest as well as at peak exercise, in patients with severe heart failure were correlated significantly to pVo2 (r = -0.77, P = 0.04; r = -0.85, P = 0.01, respectively) and to exercise duration (r = -0.72, P = 0.05; r = -0.79; P = 0.03, respectively). The relationship between plasma levels of atrial natriuretic peptide and of cGMP was shifted downward in the more severe patients suggesting the loss of biological activity of atrial natriuretic peptide.

Topics: Adult; Aged; Angiotensin II; Atrial Natriuretic Factor; Chronic Disease; Epinephrine; Exercise Test; Exercise Tolerance; Female; Heart Failure; Humans; Male; Middle Aged; Norepinephrine; Oxygen Consumption; Prognosis; Radioimmunoassay; Renin; Sensitivity and Specificity; Severity of Illness Index; Vasoconstrictor Agents; Vasopressins

Children and menstruant women are far more likely than men to develop metabolic brain damage from hyponatremia. We evaluated brain adaptation and mortality from hyponatremia in male and female rats of three different age groups. With acute hyponatremia, the mortality was 84% in prepubertal rats vs. 15% in adults and 0% in elderly rats. With chronic hyponatremia, mortality was 13% in adult males vs. 62% in females. Testosterone pretreatment significantly decreased mortality (from 62 to 9% in adult females, and from 100% to zero in prepubertal rats), but estrogen significantly increased mortality (from 13 to 44% in adult males). With acute hyponatremia in adult rats, brain sodium was significantly decreased (-17%), but in prepubertal rats it was actually increased (+ 37%). Cerebral perfusion during chronic hyponatremia was significantly impaired in adult females vs. males or controls (P < 0.01). Neither vasopressin administration nor chronic hyponatremia induced with desmopressin resulted in any mortality or decrement of cerebral perfusion. Thus age, gender, and the cerebral effects of vasopressin are major determinants of mortality in experimental metabolic encephalopathy.

Topics: Adaptation, Physiological; Aging; Animals; Brain; Brain Diseases; Chronic Disease; Estrogens; Female; Hormones; Hyponatremia; Male; Rats; Sex Characteristics; Sexual Maturation; Survival Analysis; Testosterone; Vasopressins

The influence of 1000 ml of 0.9% NaCl infusion induced hypervolemia on the water-electrolyte and hormonal balance was investigated in HBV-infected patients with chronic persistent hepatitis, chronic active hepatitis and compensated cirrhosis. All examined patients showed higher concentrations of vasopressin and atrial natriuretic peptide and the increased activity of RAA system before the trial. The induced hypervolemia caused the decrease of RAA system's activity and vasopressin concentration and increase of atrial natriuretic peptide's secretion, different in every group of patients. The latent deficiency of calcium and magnesium was found, too. The results showed that all determined patients had water-electrolyte and hormonal disorders, significantly increased in patients with chronic active hepatitis.

Topics: Adolescent; Adult; Atrial Natriuretic Factor; Calcitonin; Chronic Disease; Hepatitis B; Humans; Middle Aged; Parathyroid Hormone; Renin-Angiotensin System; Sodium Chloride; Vasopressins; Water-Electrolyte Balance

Blood contents of pressor peptide hormones vasopressin and angiotonin II were studied in patients with neuro-endocrine syndrome before and after single intake and prolonged treatment with anti-serotonin drug peritol and cholinergic agent parlodel which affect biogenic amine metabolism and, consequently, influence blood pressure. Single doses of the drugs were established to cause different blood dynamics of vasopressin and angiotonin II which classified as marked and paradoxic reactions on peritol and parlodel used separately and associatively. Fall of blood vasopressin content induced by single dose of parlodel was accompanied by blood pressure decrease. Tree-week treatment with peritol and parlodel exerted hypotensive effect and significantly reduced vasopressin blood content.

Topics: Adolescent; Adult; Angiotensin II; Biogenic Amines; Blood Pressure; Bromocriptine; Chronic Disease; Cyproheptadine; Drug Evaluation; Female; Humans; Hypertension; Hypothalamic Diseases; Male; Middle Aged; Syndrome; Time Factors; Vasopressins

Chronic osmotic stress inhibits, while repeated physical stress can increase pituitary ACTH responsiveness to a novel stress. The interaction between these effects was studied in rats subjected to repeated i.p. injection of hypertonic saline, a strong aversive stimulus with osmotic and painful and psychological stress components, for 14 days. Hypertonic saline injection caused marked drinking responses, transient increases in plasma vasopressin (VP), and marked increases in VP mRNA and irVP in magnocellular cell bodies in the hypothalamus. Parvicellular activity was also enhanced as indicated by increases in VP immunostaining in the external zone of the median eminence and CRH mRNA and irCRH in the PVN. Plasma ACTH levels increased 10-fold after 30 min hypertonic saline injection, returning to basal levels in 4 h, and there was no desensitization of the ACTH responses after repeated injections (from basal values of 76 +/- 10 to 782 +/- 57, 788 +/- 83 and 779 +/- 31 pg/ml 30 min after the first, 4th and 14th injection, respectively). Basal ACTH levels were normal 24 h after the last injection, but pituitary POMC mRNA levels were increased by 95%, and ACTH responses to a novel stress (15 min immobilization) were significantly larger than in controls (P < 0.01) despite increases in morning plasma corticosterone levels (1.5 +/- 0.4 and 9.2 +/- 3.1 micrograms/dl in controls and stressed rats, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adrenocorticotropic Hormone; Animals; Chronic Disease; Corticotropin-Releasing Hormone; Hypothalamo-Hypophyseal System; Hypothalamus; Injections, Intraperitoneal; Male; Osmotic Pressure; Pituitary-Adrenal System; Pro-Opiomelanocortin; Rats; Rats, Sprague-Dawley; RNA, Messenger; Saline Solution, Hypertonic; Stress, Physiological; Vasopressins

We describe a 71 year old man with a neurodegenerative condition who developed chronic inappropriate antidiuretic hormone secretion and hypothermia resulting in recurrent episodes of impaired consciousness. This combination of abnormalities is attributable to hypothalamic disease and has not to our knowledge been previously reported with clearly documented antidiuretic hormone excess.

Topics: Aged; Chronic Disease; Demyelinating Diseases; Humans; Hyponatremia; Hypothermia; Male; Vasopressins; Water Intoxication

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

The physiological regulation of ACTH secretion is largely dependent on the interactive effects of CRH and vasopressin (VP) in the pituitary corticotroph. The importance of the magnocellular and parvicellular hypothalamic systems as a source of VP for pituitary regulation was studied by analyzing the effects of endogenous activation of these systems or VP infusion on the ability of CRH to regulate its receptor sites in the anterior pituitary. CRH receptors were measured by binding of [125I]Tyr-ovine CRH to membrane-rich fractions of anterior and neurointermediate pituitary lobes. Minipump infusion of 100 ng/min CRH for 48 h caused a 40% decrease in the anterior pituitary CRH receptor concentration. Simultaneous infusion of VP markedly potentiated the effect of CRH, but only at doses that elevated plasma VP to levels in the range of those in the pituitary portal circulation. Activation of the magnocellular vasopressinergic system by 60 h of water deprivation increased plasma VP levels from 0.5 +/- 0.1 to 11.8 +/- 0.6 pg/ml, but had no effect on the anterior pituitary CRH receptor concentration in control rats or animals receiving CRH infusion (100 ng/min for 48 h). The CRH receptor concentration was significantly increased in neurointermediate pituitary membranes from water-deprived rats. When the parvicellular vasopressinergic system was activated by 14 days of repeated restraint stress, there was a significant enhancement in the ability of CRH to decrease anterior pituitary CRH receptors (33% and 62% in control and stressed rats, respectively). The concomitant infusion of 200 ng/min of the VP antagonist [(mercapto cyclopentamethylene propionic acid)-[methyl-tyrosine]arginine VP] during the CRH infusion in chronically stressed rats significantly reduced the magnitude of the pituitary CRH receptor loss from a 62% to a 43% decrease (P < 0.01). In conclusion, exogenous VP modulates pituitary CRH receptor regulation by CRH only at doses sufficiently high to provide peripheral VP concentrations in the range of the circulating levels in hypophysial-portal blood. Furthermore, the demonstration that chronic endogenous activation of the parvicellular, but not the magnocellular, vasopressinergic system enhances the down-regulatory effect of CRH on anterior pituitary CRH receptors is in support of a critical role of parvicellular VP in the control of the corticotroph function.

Topics: Adrenocorticotropic Hormone; Animals; Chronic Disease; Corticotropin-Releasing Hormone; Down-Regulation; Male; Pituitary Gland; Rats; Rats, Sprague-Dawley; Receptors, Corticotropin-Releasing Hormone; Stress, Physiological; Vasopressins; Water Deprivation

Overall 210 patients aged 60-74 years suffering from coronary heart disease associated with chronic circulatory failure, stages I, IIA and IIB, 53 patients aged 45-59 years and 20 healthy persons aged 45-74 years were examined for the renin-angiotensin-aldosterone system and antidiuretic hormone. Renin activity, the concentration of aldosterone and vasopressin in blood plasma were investigated by radioimmunoassay. In the initial stage of heart failure, the elderly persons showed up more marked renin activation in blood plasma, followed by its lowering as decompensation progressed as well as an increase in the concentration of aldosterone and vasopressin, which resulted in the progress of circulatory failure.

Topics: Aged; Aldosterone; Chronic Disease; Female; Heart Failure; Humans; Male; Middle Aged; Renin; Renin-Angiotensin System; Sex Characteristics; Vasopressins

In patients with congestive heart failure (CHF), overactivity of the sympathetic nervous system may be accompanied by an impairment of the baroreflex control mechanism. To evaluate the reflex responses of the sympathetic nervous system, the renin-angiotensin system and vasopressin release to baroreceptor unloading, 38 patients with left ventricular dysfunction were studied. Hemodynamic data, and plasma norepinephrine, renin activity and vasopressin concentrations were measured before and 60 minutes after administration of high-dose hydralazine (0.4 mg/kg intravenously). On the basis of blood pressure response to vasodilator administration, patients were divided arbitrarily into those with a decrease in mean arterial blood pressure greater than or equal to 15 mm Hg (group A; n = 12) and those with a decrease less than 15 mm Hg (group B; n = 26) compared with control values. In response to hydralazine, heart rate decreased in group A from 100 to 92 beats/min (p less than 0.001) and increased in group B from 90 to 96 beats/min (p less than 0.05). In group A, hemodynamic changes induced by hydralazine were accompanied by a decrease in plasma norepinephrine from 822 to 518 pg/ml (p less than 0.01) and an increase in plasma vasopressin from 8.4 to 45.2 pg/ml (p less than 0.001). In group B, plasma norepinephrine and vasopressin did not change significantly (407 vs 447, and 8.4 vs 8.3 pg/ml, respectively). Plasma renin activity remained unchanged in group A and increased in group B (p less than 0.001). The data show that baroreceptor-mediated release of vasopressin is not impaired in patients with CHF and a defective sympathetic reflex control mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Cardiac Catheterization; Chronic Disease; Female; Heart Failure; Hemodynamics; Humans; Hydralazine; Male; Middle Aged; Norepinephrine; Pressoreceptors; Renin; Sympathetic Nervous System; Vasopressins

Plasma cortisol, prolactin and vasopressin concentrations were measured by radioimmunoassay in blood samples from control and lame sheep. The lame sheep were all suffering from naturally occurring clinical cases of footrot and showed all the behavioural characteristics of chronic pain; they were scored for impairment of gait and pathology of the foot and divided into mild and severely lame groups. The severely lame sheep had increased plasma prolactin and decreased plasma cortisol concentrations. Plasma vasopressin was variable and showed no consistent changes with lameness. The relationships between plasma cortisol, prolactin and vasopressin may be a useful index in the assessment of animals experiencing chronic pain, when taken in conjunction with other measurements.

Topics: Animals; Chronic Disease; Female; Foot Rot; Hydrocortisone; Lameness, Animal; Pain; Prolactin; Radioimmunoassay; Sheep; Sheep Diseases; Vasopressins

Assessment of vasopressin by radioimmunoassay has shown an increase in its blood concentration and a disturbed reaction of the vasopressinergic structures of the hypothalamus to metoclopramide, furosemide, insulin hypoglycemia, and exercise. Functional tests with the dopaminergic drug bromocriptine and antiserotoninergic drug cyproheptadine help to make an individual choice of the most effective drug for therapy of the hypothalamic syndrome of neuroendocrine-metabolic type. The patients can be divided into sensitive to either the first or the second drug of both which is important for adequate pathogenetic therapy.

Topics: Adolescent; Adult; Chronic Disease; Exercise Test; Humans; Hypothalamic Diseases; Hypothalamo-Hypophyseal System; Middle Aged; Pituitary Gland, Posterior; Radioimmunoassay; Syndrome; Time Factors; Vasopressins

We evaluated the changes in the hepatic hemodynamics and blood ketone body ratio (KBR) induced by vasopressin in 40 patients with chronic liver diseases to clarify the effect of hepatic blood flow on hepatic energy charge expressed by KBR. Following infusion of vasopressin, the rate of decrease in portal blood flow in liver cirrhosis (LC) was significantly lower than that in chronic hepatitis (CH). Moreover, the blood flow in the hepatic artery after vasopressin infusion was greater in LC than in CH. As a result, the total hepatic blood flow, which was the sum of the flow in the above two vessels, after vasopressin infusion was greater in LC than in CH but the decrease in the blood KBR was not significant in LC. Thus, vasopressin appears to be hemodynamically safe in patients with LC, but caution is needed since it may decrease blood pressure, total hepatic blood flow and KBR in some LC patients.

Topics: Adult; Chronic Disease; Energy Metabolism; Hemodynamics; Humans; Infusions, Intravenous; Ketone Bodies; Liver; Liver Circulation; Liver Diseases; Middle Aged; Vasopressins

We reported two infants with hydranencephaly and chronic hypernatremia. Their plasma sodium concentration gradually increased during the first week and remained between 150-160 mEq/L thereafter. They showed no signs of thirst. A water deprivation test demonstrated low urine osmolality and low plasma ADH concentration despite markedly elevated plasma osmolality in both cases. Urine was significantly concentrated when vasopressin was given. Thus, it was concluded that both thirst mechanism and ADH secretion were disturbed in these two cases. ADH producing cells, the thirst center and the osmoreceptor are all located in the hypothalamus. Radiographic measures showed dysplasia of the hypothalamus, providing the anatomical basis for their dysfunction.

Topics: Anencephaly; Chronic Disease; Female; Humans; Hydranencephaly; Hypernatremia; Infant, Newborn; Sodium; Vasopressins

Herein we will describe a case of chronic hypernatremic-hyperosmolar syndrome with cerebral localization of systemic sarcoidosis. Several determinations of plasma arginine vasopressin (p-AVP) at various plasma sodium levels were carried out in this patient. During the study p-AVP values varied between 2.6 and 9.5 pg/ml. A high percentage of them was related to plasma osmolality, pointing out that p-AVP secretion was osmotically mediated. This behavior is in contrast with the tendency of hypernatremic patients previously reported in the literature, in whom p-AVP values were inappropriately low for the corresponding degree of plasma osmolality, suggesting that vasopressin secretion was not influenced by osmotic stimulation. Furthermore, our case, unlike those previously described, showed high values of urinary osmolality. In conclusion, our patient represents, in essence, the 'middle' of the spectrum of the hypodipsic-hypernatremic syndrome, because she is to be inserted between the majority of patients who have little or no osmotically mediated AVP release and the case of a child, recently described, who had completely normal AVP secretion.

Topics: Arginine Vasopressin; Brain Diseases; Chronic Disease; Female; Humans; Hypernatremia; Middle Aged; Osmolar Concentration; Sarcoidosis; Syndrome; Thirst; Vasopressins

The dynamics of the content of blood aldosterone and vasopressin after hemosorption studied in 17 patients with decompensated chronic cor pulmonale revealed a significant reduction of their concentration. Reduction of the content of hormones in the blood occurred due to the effect of the sorbent and is not related to the influence of heparine.

Topics: Adult; Aldosterone; Chronic Disease; Drug Interactions; Female; Heart Failure; Hemoperfusion; Heparin; Humans; Male; Middle Aged; Pulmonary Heart Disease; Vasopressins

The aim of this paper was to study atrial natriuretic factor, plasma renin activity and antidiuretic hormone values during paroxysmal atrial arrhythmias with different ventricular rates before and after pharmacological cardioversion and during chronic atrial flutter-fibrillation. The study was carried out: 1) during acute arrhythmias (atrial flutter-fibrillation or supraventricular tachycardia) and after restoration of normal sinus rhythm in 2 patients without heart disease, in 13 with chronic heart disease and in 6 with acute myocardial infarction; 2) during chronic atrial flutter-fibrillation in 5 patients with chronic ischemic heart disease, without congestive heart failure. Atrial natriuretic factor, aldosterone, plasma renin activity and antidiuretic hormone values were measured by radio-immunoassay. During paroxysmal atrial arrhythmias atrial natriuretic factor levels were higher than normal in all patients, particularly in those with supraventricular tachycardia. Most of the aldosterone measurements were above the normal range. As far as plasma renin activity and antidiuretic hormone values are concerned, levels higher than the normal range were found in the patients with severe hemodynamic impairment. Central venous pressure was above normal in all patients except in the 2 without heart disease, and there was a positive correlation between atrial natriuretic factor and central venous pressure values. After restoration of normal sinus rhythm atrial natriuretic factor values returned to normal except in acute myocardial infarction patients, in 1 chronic ischemic heart disease patient with congestive heart failure and in 3 patients with mitral valve disease. In all patients with chronic atrial flutter-fibrillation and in 5 patients with acute atrial flutter-fibrillation and low rate, above normal atrial natriuretic factor values were found with normal central venous pressure values. Atrial distension due to high central venous pressure values, lack of atrial contraction and rhythmic detension of the atrial stretch receptors, may be considered the major stimuli responsible for atrial natriuretic factor release during acute paroxysmal atrial arrhythmias and atrial flutter-fibrillation with low ventricular rate, respectively.

Topics: Acute Disease; Adult; Aged; Aldosterone; Atrial Fibrillation; Atrial Flutter; Atrial Natriuretic Factor; Blood Pressure; Central Venous Pressure; Chronic Disease; Female; Humans; Male; Middle Aged; Renin; Tachycardia, Supraventricular; Vasopressins

Topics: Chronic Disease; Clinical Laboratory Techniques; Female; Humans; Hyponatremia; Kidney; Middle Aged; Osmolar Concentration; Referral and Consultation; Urodynamics; Vasopressins

The role of vasopressin in the regulation of body water volume and its distribution to intravascular, interstitial and intracellular compartments, and the importance of particular body water compartments in the pathogenesis of DOCA-salt hypertension were studied in young Brattleboro rats. Vasopressin-deficient, vasopressin-synthesizing and vasopressin-deficient rats chronically supplemented with deamino-8-D-arginine vasopressin (dDAVP) were compared with water-drinking controls. The chronic DOCA-salt treatment caused a marked hypertension in vasopressin-synthesizing animals; in these animals body water was slightly increased due to the expansion of extra-cellular fluid volume whereas intracellular water tended to decrease, so that the ratio of extracellular fluid volume to intracellular water rose significantly. The development of DOCA-salt hypertension was attenuated in the vasopressin-deficient rats, which had a similar level of total body water, slightly increased intracellular water and significantly decreased extracellular fluid volume compared with the hypertensive vasopressin-synthesizing rats. Consequently, in the vasopressin-deficient rats, the ratio of extracellular fluid volume to intracellular water did not differ from that of controls. A vasopressin deficiency was associated with a failure to expand the interstitial fluid volume although plasma volume was increased. Unaltered total body water together with elevated plasma osmolality indicated an extracellular water deficiency in DOCA-salt-treated vasopressin-deficient rats. Chronic dDAVP supplementation restored the body fluid pattern and the hypertensive response of the DOCA-salt-treated vasopressin-deficient rats. In conclusion, the antidiuretic effects of vasopressin are necessary for the interstitial fluid volume expansion that is essential for a full development of DOCA-salt hypertension.

Topics: Animals; Body Water; Chronic Disease; Deamino Arginine Vasopressin; Desoxycorticosterone; Heterozygote; Homozygote; Hypertension; Nephrectomy; Rats; Rats, Brattleboro; Sodium Chloride; Vasopressins

Plasma ADH, PA and PRA in patients with respiratory failure (RF) were studied. RF patients were divided into 4 groups, i.e. acute RF (ARF) and chronic RF (CRF), with or without hypercapnia. The levels of these hormones were significantly higher in RF than those in control subjects, moreover, they were markedly elevated in ARF than those in CRF. In multiple regression analysis, ADH correlated with PaO2, pH and PRA in RF patients, but correlated with serum osmolality in control subjects. It was considered that ADH in RF was affected by the direct effect of blood gases and circulatory disorder. The mechanism of elevated PA and PRA in RF probably was mediated through restriction of intake of water and Na, reduction of renal blood flow and decreased ACE often occurred in RF. Abnormally elevated hormones are more often recognized in edematous patients than in nonedematous patients. It was suggested that many patients with RF develop heart failure or edema due to hormonal abnormalities.

Topics: Acute Disease; Aged; Aldosterone; Chronic Disease; Female; Humans; Male; Middle Aged; Renin; Respiratory Insufficiency; Vasopressins

Plasmapheresis (PP) was used in 28 patients with medication-resistant high arterial hypertension (AH). PP-induced changes in plasma renin activity and blood aldosterone, angiotensin II and antidiuretic hormone levels of patients with high AH are shown to be a compensatory-adaptive response, maintaining homeostasis. PP sessions (27 ml/kg body weight at a rate of 0.22 ml/kg/min, at the maximum) do not produce renin-angiotensin-aldosterone activation. Long-term hypotensive effect of PP in cases of high AH might be related to a gradual decrease in blood angiotensin II and systemic aldosterone synthesis. It is suggested that the hypotensive effect of PP may be due to an intricate interaction of effects, with humoral, receptor and circulatory re-adjustments of arterial BP control being the most prominent among those.

Topics: Adult; Chronic Disease; Drug Resistance; Female; Humans; Hypertension; Hypertension, Malignant; Male; Middle Aged; Plasmapheresis; Renin-Angiotensin System; Time Factors; Vasopressins

Our results reviewed here may be summarized as follows: 1. Continuous endotoxemia significantly interferes with Ca2+-dependent information flow in the liver. 2. The subcellular sites where these molecular lesions can be localized include: a.) the plasma membrane-there are effects at the level of alpha 1-adrenergic and vasopressin binding, and also in the coupling of receptor activation to inositol lipid metabolism in terms of PIP2 degradation and resynthesis b.) the endoplasmic reticulum in terms of Ca2+ release and PI synthesis. Another one of the sequelae of Ca2+-associated receptor activation, namely, cytosolic ionized Ca2+ concentration is also affected. 3. Finally, in addition to seeing the impact of acute or continuous endotoxemia at the level of receptor activation and signal generation, we can also document alterations in the expression of physiologic function subserved by these Ca2+- and inositol lipid-associated signaling processes--i.e. in glycogen phosphorylase activity-being consistent with the above described changes. In conclusion, we state that a causal link is shown between receptor binding, agonist-induced phosphoinositide hydrolysis, intracellular Ca2+ mobilization and activation of phosphorylase a in the liver, suggesting that these alterations may underlie some of the metabolic consequences of chronic sepsis.

Topics: Acute Disease; Animals; Calcium; Cell Membrane; Chronic Disease; Endotoxins; Escherichia coli; Liver; Male; Phosphatidylinositols; Phosphorylase a; Rats; Rats, Inbred Strains; Receptors, Adrenergic, alpha; Receptors, Angiotensin; Receptors, Vasopressin; Vasopressins

Topics: Adult; Aged; Chronic Disease; Epinephrine; Female; Heart Failure; Hemodynamics; Humans; Male; Middle Aged; Norepinephrine; Physical Exertion; Renin; Vasopressins

The effects of vasopressin on colonic motility were investigated in 6 healthy subjects and 10 patients with chronic idiopathic constipation. Recordings of the colonic myoelectric spiking activity were performed by means of 50-cm long silastic tube, equipped with four bipolar ring electrodes fixed at 10-cm intervals, which was introduced by flexible colonoscopy into the left colon. Tracing were obtained for 1 h in the fasting state and for another hour after an intramuscular injection of a pharmacological dose of vasopressin (0.3 U/kg). The different types of spike bursts generated by the colonic smooth muscle were compared before and after vasopressin injection. In both controls and patients, the tracing showed (i) rhythmic stationary spike bursts (RSB) that were seen at only one electrode site; and (ii) sporadic bursts that were either propagating over all four electrodes (SPB) or nonpropagating (SNPB). Injection of vasopressin in controls was followed for 30 min by a significant increase in the number of propagating bursts from 2.7 +/- 0.6 (mean +/- SEM) to 5.2 +/- 1.4 bursts (p less than 0.05); RSB and SNPB were not altered by vasopressin. In the constipated patients, the number of propagating bursts during the control period was significantly lower (0.8 +/- 0.2 bursts/30 min) than in the volunteers (p less than 0.05). After vasopressin, there was a significant increase to 3.6 +/- 0.8 bursts/30 min (p less than 0.001); RSB and SNPB also did not show significant alteration after vasopressin. Finally, 4 out of the 10 patients passed stools during the recording session.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Chronic Disease; Colon; Constipation; Electromyography; Electrophysiology; Female; Gastrointestinal Motility; Humans; Male; Peristalsis; Vasopressins

Topics: Aged; Blood Pressure; Chronic Disease; Female; Hemodynamics; Humans; Liver Circulation; Liver Cirrhosis; Male; Middle Aged; Portal System; Propranolol; Vasopressins

Blood vasopressin, tri-iodothyronine, total thyroxine, thyrotrophic hormone, cortisol, ACTH and insulin levels were measured in 60 chronic coronary patients aged 35 to 70. Coronary patients showed elevated blood vasopressin, particularly in the presence of frequently recurring anginal attacks. There was no significant difference in vasopressin levels of patients with and without attendant essential hypertension, those with atherosclerotic and postinfarction cardiosclerosis, or in relation to body weight. Insulin, cortisol, adrenocorticotrophic and thyrotrophic hormones were significantly increased, and tri-iodothyronine and total thyroxine, significantly decreased, in coronary patients as compared to the controls.

Topics: Adrenocorticotropic Hormone; Adult; Aged; Chronic Disease; Coronary Disease; Humans; Hydrocortisone; Insulin; Male; Middle Aged; Thyroid Hormones; Vasopressins

Inoculation of rats at the tail-base with Mycobacterium led to arthritic swelling and inflammation of all four limbs. Immunoreactive (ir)-dynorphin (DYN) increased in anterior but not neurointermediate pituitary. In the brain, only thalamus showed a rise and, in spinal cord, a large elevation was seen. Ir-vasopressin (VP) was not affected in these tissues but increased in midbrain. These effects might reflect a role of DYN in the control of chronic pain. In addition, they support a differential modulation of DYN as compared to VP extrinsic to the hypothalamic-neurohypophyseal axis.

Topics: Animals; Central Nervous System; Chronic Disease; Dynorphins; Mesencephalon; Pain; Pituitary Gland, Anterior; Rats; Spinal Cord; Thalamus; Vasopressins

To elucidate the effect of bed rest used as an adjunct to increased diuretic treatment, twelve patients with chronic congestive heart failure (CHF) had a 50% increase in loop diuretic dosage and were allocated to either continuous bed rest or bed rest during nights only. The 24-hour bed rest group reduced their weight significantly (mean +/- SEM: 2.00 +/- 0.79 kg, P less than 0.001), whereas the night bed rest group had no significant weight reduction (1.10 +/- 0.37 kg, 0.1 less than P less than 0.2) during three days of observation. Furthermore, the 24-hour bed rest group had a significantly increased diuresis (P less than 0.05) during the first day of the study and a tendency towards increased natriuresis. The cumulated diuresis for the two groups (24-hour bed rest versus night bed rest) during the three days of study were 7773 +/- 700 ml and 5861 +/- 909 ml (0.05 less than P less than 0.1), respectively. Plasma concentrations of adrenaline, noradrenaline, renin and aldosterone were increased, as measured in the supine position. No significant differences were found between the two groups. Plasma concentrations of antidiuretic hormone were within normal limits. In conclusion, continuous bed rest is a reasonable adjunct to diuretic treatment in patients with CHF.

Topics: Adult; Aged; Aldosterone; Bed Rest; Body Weight; Chronic Disease; Combined Modality Therapy; Diuretics; Epinephrine; Female; Heart Failure; Humans; Male; Middle Aged; Natriuresis; Norepinephrine; Posture; Prospective Studies; Renin; Vasopressins

Rats inoculated in the tail-base with killed Mycobacterium butyricum developed an arthritic swelling and inflammation of the limbs accompanied by a hyperalgesia to noxious pressure applied thereto. These changes were maximal at 3 weeks and had subsided by 10 weeks post-inoculation. At 3 weeks, arthritic rats manifested an elevation in levels of immunoreactive (ir)-vasopressin (VP) but not ir-oxytocin (OT) in the midbrain. In contrast, ir-OT was increased in the medulla-pons while ir-VP was unaltered therein. These changes had disappeared by 10 weeks. No other brain region displayed changes. Thus, chronic arthritis is associated with selective and reversible effects upon discrete brain pools of ir-VP and ir-OT. The data clearly demonstrate that pools of ir-VP and ir-OT can be modulated independently of each other in particular brain tissues. Whether the changes are produced by, or reflect a functional response to, the pain rather than other characteristic of the arthritis, remains to be determined.

Topics: Animals; Arthritis; Arthritis, Experimental; Brain Chemistry; Chronic Disease; Male; Oxytocin; Pain; Rats; Rats, Inbred Strains; Stress, Physiological; Vasopressins

The effects of administration of angiotensin II (ANG II) and antidiuretic hormone (ADH) on the glomerular filtration rate (GFR, measured as creatinine clearance) were examined in patients with mesangial proliferation. For this study, the patients whose conditions were similar to that of healthy subjects, except for asymptomatic urinary abnormalities and glomerular histological changes, were selected. Both ANG II and ADH administration significantly decreased GFR in the patients and the healthy subjects. Compared to the healthy subjects, a significantly greater drop in GFR was observed in the patients following ANG II infusion with or without SQ14225 administration, but not following ADH infusion. We conclude that mesangial proliferation may modulate an ANG II induced drop in GFR.

Topics: Adult; Angiotensin II; Blood Pressure; Chronic Disease; Creatinine; Glomerular Filtration Rate; Glomerular Mesangium; Glomerulonephritis; Humans; Kidney Function Tests; Male; Natriuresis; Urine; Vasopressins

Topics: Administration, Intranasal; Adult; Carbamazepine; Chlorpropamide; Chronic Disease; Deamino Arginine Vasopressin; Diabetes Insipidus; Diuresis; Drug Evaluation; Humans; Pituitary Hormones, Posterior; Vasopressins

The concentration of aldosterone in blood plasma of rats with chronic water and restricted sodium chloride intake substantially rose after subcutaneous injection of the antidiuretic hormone pituitrin in physiological doses. No simultaneous increase in blood corticosterone was seen. The production of hormones by rat adrenals remained unchanged. The results of experiments made with ACTH alone or combined with pituitrin permitted the conclusion that the increase in aldosterone concentration was not linked with a possible stimulation of endogenous ACTH secretion. The augmentation of aldosterone concentration in the peripheral blood of rats with chronic water intake induced by pituitrin is likely to be due to a decrease in metabolic clearance of the hormone.

Topics: Adrenocorticotropic Hormone; Aldosterone; Animals; Chronic Disease; Corticosterone; Diet, Sodium-Restricted; Male; Pituitary Hormones, Posterior; Rats; Vasopressins; Water Intoxication

An increased activity of vasoconstrictor mechanisms may play an important role in circulatory adjustments to heart failure. Thus, hemodynamic data and the plasma hormones epinephrine (E), norepinephrine (NE) and arginin vasopressin (AVP) as well as the plasma renin activity (PRA) were assessed in 50 patients undergoing coronary angiography and right heart catheterization. Patients were classified into three groups according to severity of left ventricular (LV) dysfunction as assessed by ejection fraction (LVEF): those with normal left ventricular function (group 1 (n = 12): LVEF greater than or equal to 55%, mean 70 +/- 3%) and those with moderate (group 2 (n = 16): LVEF 54-35%, mean 43 +/- 2%) or severe LV dysfunction (group 3 (n = 22): LVEF less than 35%, mean 22 +/- 1%). At rest plasma NE concentrations in patients with heart failure (group 2: 187 +/- 17 pg/ml; group 3: 299 +/- 27 pg/ml) did not differ significantly from control values (199 +/- 26 pg/ml). During exercise, NE concentrations increased in all patients (p less than 0.001). This increase in plasma NE was more pronounced in group 3 (753 +/- 71 pg/ml) than in group 1 (262 +/- 37) and group 2 (388 +/- 64). A significant inverse correlation was found between plasma NE and stroke index at rest (r = -0.592, p less than 0.001) as well as during exercise (r = -0.659, p less than 0.001). PRA was elevated at rest and during exercise in patients of group 3 but not of group 2 as compared with control patients (p less than 0.05). Plasma E and AVP were similar in all groups. Patients of group 3 were subdivided according to exercise capacity into patients who tolerated a maximum work load of 50 watts or more (group 3A) and those who did not tolerate a work load exceeding 25 watts (group 3B). At rest and during exercise, patients of group 3A had a higher stroke index than patients of group 3B. In contrast, there was no significant difference in LVEF between group 3A and 3B (22 +/- 2 vs 20 +/- 1%). During exercise patients with low exercise capacity (group 3B) had higher NE levels than patients with less impaired exercise capacity (group 3A) (948 +/- 86 vs 590 +/- 65 pg/ml, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Chronic Disease; Coronary Vessels; Epinephrine; Female; Heart Failure; Heart Ventricles; Hemodynamics; Humans; Male; Norepinephrine; Renin; Sodium; Vasoconstriction; Vasoconstrictor Agents; Vasopressins

Lesions of the hypothalamic paraventricular nucleus depleted immunoreactive (ir)-vasopressin (VP) and -oxytocin (OT) from rat spinal cord but failed to modify nociceptive thresholds. Further, intrathecal introduction of VP and OT into the cord failed either to influence nociceptive thresholds or to modify the antinociceptive action of morphine. However, doses of VP as low as 20 ng caused, in contrast to OT, a hind-limb muscular flaccidity and respiratory disturbances. Rats suffering from chronic arthritis did not, finally, reveal any alterations in levels or ir-VP or ir-OT in the spinal cord. Is is concluded that spinal pools of VP and OT are derived from the paraventricular nucleus and do not play a major role in nociceptive processes in the spinal cord. A role of spinal VP in motor and, possibly autonomic control is, nevertheless, indicated.

Topics: Animals; Arthritis, Experimental; Chronic Disease; Male; Morphine; Oxytocin; Pain; Paraventricular Hypothalamic Nucleus; Rats; Rats, Inbred Strains; Sensory Thresholds; Spinal Cord; Vasopressins

Topics: Aldosterone; Angiotensin II; Blood Pressure; Chronic Disease; Humans; Hypernatremia; Male; Middle Aged; Renin; Vasopressins

Angiography is of value in the diagnosis and interventional therapy of diffuse hepatocellular disease. Hepatic arteriography is the primary diagnostic method; hepatic venography, portal venography, transvenous liver biopsy and direct cholangiography are complementary. They allow the assessment of type and stage of diseases, their hemodynamic consequences and permit the differentiation of diffuse diseases from tumorous processi. Selective vasopressin infusion and transhepatic catheter obliteration of varices are interventional techniques used to control massive bleeding from gastroesophageal varices--one of the most serious complications of diffuse hepatocellular diseases.

Topics: Acute Disease; Angiography; Budd-Chiari Syndrome; Cholangiography; Chronic Disease; Embolization, Therapeutic; Esophageal and Gastric Varices; Hepatic Veins; Hepatitis; Hepatitis, Alcoholic; Hepatitis, Viral, Human; Humans; Liver Cirrhosis; Phlebography; Portal Vein; Vasopressins

Topics: Acute Disease; Carbamazepine; Chlorpropamide; Chronic Disease; Clofibrate; Diabetes Insipidus; Diagnosis, Differential; Humans; Saline Solution, Hypertonic; Vasopressins

Two patients ( 1 7/12-year-old and 1 11/12-year-old girls) with chronic hypernatremia were studied. Neuroradiological findings and mildine facial defects showed characteristic features of holoprosencephaly. Water deprivation tests showed clear evidence of antidiuretic hormone (ADH) secretion. The responses to hypertonic saline infusion and acute water loading were abnormal. In one case, the impaired osmotic regulation of ADH secretion was demonstrated by measuring urinary ADH by a radioimmunoassay. In this case, the volume regulation of ADH secretion seemed to be also incomplete since chronic water loading for a period of six days induced water retension.

Topics: Brain; Cerebral Angiography; Chronic Disease; Female; Humans; Hypernatremia; Infant; Osmolar Concentration; Saline Solution, Hypertonic; Tomography, X-Ray Computed; Vasopressins; Water

The blood vasopressin content and kinin system activity were studied in 83 patients with chronic ischemic heart disease of various severity. It was established that the blood vasopressin concentration increases with an increase in the severity of the disease. A high degree of correlation between changes in vasopressin content and in components of the kinin system was revealed: increase in the concentration of vasopressin is attended by activation of the kallikrein-kinin system. The mechanisms of the interrelationship of the vasopressin and kinin content are discussed. It is suggested that vasopressin may play a role in the pathogenesis of chronic ischemic heart disease.

Topics: Adult; Chronic Disease; Coronary Angiography; Coronary Disease; Esterases; Humans; Kallikreins; Kinins; Lysine Carboxypeptidase; Middle Aged; Vasopressins

The hypothalamohypophyseal neurosecretory system (HHNS) was examined in the deceased from myocardial infarctions and chronic cardiac insufficiency. All 80 cases of infarctions showed in increased functional activity of the HHNS, irrespective of the time from the beginning of the disease. If the infarction was complicated by decompensation, the HHNS was characterized by hypervasopressure accompanied by occurrence of small vacuolized cells in the supraoptical nuclei with a low secretion content and high activity of biosynthetical enzymes, and a drop of secretion in the neurohypophysis. In chronic cardiac insufficiency (50 cases) there were 2 variants of changes in the HHNS, which correlated with the level of sympathetic nervous system activity (which was vitally determined from the diurnal catecholamine excretion). With high sympathetic activity, the changes in the HHNS were identical to those in myocardial infarctions, complicated by decompensation. The low activity was associated with HHNS depletion, which correlated with patients' nonsusceptibility to pathogenetic therapy.

Topics: Acute Disease; Chronic Disease; Glutamate Dehydrogenase; Heart Failure; Humans; Hypothalamo-Hypophyseal System; Myocardial Infarction; NADPH Dehydrogenase; Potassium; Sodium; Sympathetic Nervous System; Vasopressins

We evaluated demeclocycline and lithium therapy in 10 patients with the syndrome of inappropriate secretion of antidiuretic hormone. Despite severe water restriction, all patients had hyponatremia (mean +/- S.E.M. serum sodium of 122 +/- 1.1 meq per liter) and elevated urine osmolality (744 +/- 59 mOsm per kilogram) before treatment. Demeclocycline (600 to 1200 mg daily) restored serum sodium concentration to 139 +/- 1.1 meq per liter within five to 14 days, permitting unrestricted water intake in all patients. In three patients given lithium carbonate (900 mg daily) the serum sodium concentration, urine osmolality and urine volume were unchanged; since two patients had adverse central-nervous-system symptoms during lithium therapy, further study of this agent was abandoned. A patient with an unusual 22-year history of the syndrome was unresponsive to lithium, whereas long-term treatment with demeclocyline was markedly effective. Demeclocycline is superior to lithium in the treatment of the syndrome and may obviate the need for severe water restriction.

Topics: Adult; Aged; Child; Chronic Disease; Demeclocycline; Drug Evaluation; Female; Humans; Hyponatremia; Lithium; Male; Middle Aged; Osmolar Concentration; Sodium; Syndrome; Vasopressins

The efficacy of demeclocycline hydrochloride in suppressing the tubular action of tumoral antidiuretic products was tested in seven patients with the syndrome of inappropriate antidiuretic hormone secretion. In all patients, demeclocycline hydrochloride (1,200 mg/day) induced production of hypotonic urine and corrected hyponatremia despite large fluid intakes. Comparison of the response to a standard water load before and during treatment showed a notable improvement in the response to water ingestion. Even though demeclocycline moderately impairs renal function, it appears to be the treatment of choice in the chronic form of the syndrome.

Topics: Administration, Oral; Aged; Carcinoma, Small Cell; Chronic Disease; Demeclocycline; Depression, Chemical; Dose-Response Relationship, Drug; Humans; Hyponatremia; Kidney Concentrating Ability; Lung Neoplasms; Male; Middle Aged; Syndrome; Vasopressins

Over a four-year period, eight patients with documented gastrointestinal bleeding had angiography as a part of their investigation and treatment at the Department of Radiology, Victoria General Hospital, Halifax, Nova Scotia. A review of these eighty cases has been carried out and angiography has been found to be both safe and reliable in the diagnosis of gastrointestinal bleeding. Cautiously administered intra-arterial pitressin infusion therapy will arrest bleeding in about one-third of cases and in most others will reduce blood loss so that a critically ill patient may be made more fit for subsequent surgery. Patients who have recently received intravenous pitressin should not be given intra-arterial pitressin.

Topics: Aged; Angiography; Chronic Disease; Diagnostic Errors; Female; Gastrointestinal Hemorrhage; Humans; Injections, Intra-Arterial; Male; Middle Aged; Rectum; Vasopressins

Topics: Aldosterone; Angiotensin II; Arginine Vasopressin; Carbon Dioxide; Chronic Disease; Humans; Kidney; Lung Diseases, Obstructive; Osmolar Concentration; Renin; Sodium; Vasopressins; Water

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

A case of a massive colonic hemorrhage in nontoxic, quiescent ulcerative colitis is described. The source of active colonic bleeding was primarily defined with selective superior mesenteric arteriography and was completely controlled with transcatheter vasopressin infusion. A suubsequent elective segmental distal transverse and descending colectomy revealed chronic ulcerative colitis; localized marked inflammatory giant pseudopolyp formation near the splenic flexure was responsible for the bleeding.

Topics: Aged; Chronic Disease; Colitis, Ulcerative; Colonic Diseases; Female; Gastrointestinal Hemorrhage; Humans; Radiography; Vasopressins

Topics: Acute Disease; Angiography; Chronic Disease; Contrast Media; Gastrointestinal Hemorrhage; Humans; Male; Middle Aged; Vasopressins

In 11 conscious normovolaemic patients with acute or chronic pancreatitis the effect of a continuous intravenous infusion of lysine-8-vasopressin, 5 IU/70 kg b.w./20 min on the portal and the hepatic venous blood flows was studied by using multiple portal catheters, oxygen saturation measurements and an indicator dilution technique with continuous infusion of 133Xe into the portal vein or its tributaries. During vasopressin infusion the total hepatic blood flow, estimated by the Bradley technique with indocyanine green dye, was reduced to 61% of the value at rest. Owing to the simultaneously occurring streamlining of the portal venous flow with incomplete mixing of indicator and blood, the portal and hepatic venous blood flows could be measured in only 3 of 9 patients. The reduction in the portal venous blood flow during vasopressin infusion was more marked than the decrease of the total hepatic flow, corresponding to a calculated increase of the hepatic arterial flow of 50%. Total splanchnic oxygen uptake and extrahepatic splanchnic oxygen uptake were unchanged during and after infusion of vasopressin. Thus, changes in splandhnic blood flow could be estimated from changes in arteriovenous oxygen differences. Also by this method a more pronounced reduction in the portal venous than of the hepatic venous blood flow was observed. The decrease during vasopressin infusion of the superior mesenteric venous flow was more marked than that of the splenic vein. The splanchnic circulatory changes may be different for other doses of vasopressin and in cirrhotic patients with higher hepatic arterial blood flow fractions.

Topics: Acute Disease; Adult; Chronic Disease; Female; Humans; Injections, Intravenous; Liver Circulation; Male; Middle Aged; Oxygen Consumption; Pancreatitis; Partial Pressure; Vasopressins

Impaired water excretion has been described in stable, nonedematous patients with chronic obstructive lung disease (COLD). To elucidate the mechanism involved, we measured basal glomerular filtration rate (GFR), effective renal plasma flow (ERPF), and water, sodium, and solute excretion for 4 hours after water loading (20 ml. per kilogram orally or as D5W intravenously) in two groups of 10 age-matched, hypoxic, stable, nonedematous COLD normocapneic and hypercapneic patients (PCO2 less than or greater than 45 mm. Hg, respectively). In 5 patients of each group, additional measurements of plasma and urine osmolality and plasma vasopressin were made at 30-minute intervals after oral water loading and the results compared to those obtained in 10 normal control subjects. Hypoxic (PO2 61 plus or minus 2 mm. Hg), normocapneic (PCO2 39 plus or minus 1 mm. Hg) patients had normal GFR (114 plus or minus 5 ml. per minute) and ERPF (517 plus or minus 31 ml. per minute) and excreted the load normally (101 plus or minus 5 per cent of oral or intravenous water per 4-hours). This was associated with a normal rate of sodium excretion (34 plus or minus 5 mEq. per 4-hours) and low-normal plasma vasopressin (1.9 plus or minus 0.7 pg. per milliliter) which was suppressed appropriately with water loading. Hypercapneic (PCO2' 62 plus or minus 5), hypoxic (PCO2' 57 plus or minus 2) patients had normal GFR (106 plus or minus 7), low baseline vasopressin (1.1 plus or minus 0.2) which was suppressed appropriately, and decreased (p less than 0.05) 4-hour water excretion (63 plus or minus 8 per cent), 4-hour sodium excretion (15 plus or minus 9), and ERPF (394 plus or minus 31). A significant correlation was observed between impaired water and impaired sodium excretion (p less than 0.05). These studies indicate that in COLD patients: (1) hypercapnia but not hypoxemia is related to the abnormal water handling and to the increased reabsorption of sodium by the renal tubule; (2) the defect in water excretion is not related to abnormal vasopressin secretion or metabolism; (3) the alteration in sodium excretion may be due to hypercapneic-induced increase in renal bicarbonate reabsorption and/or abnormal renal blood flow.

Topics: Adult; Arginine; Chronic Disease; Glomerular Filtration Rate; Humans; Hypercapnia; Hypoxia; Kidney; Lung Diseases, Obstructive; Middle Aged; Osmolar Concentration; Radioimmunoassay; Regional Blood Flow; Regression Analysis; Sodium; Urine; Vasopressins; Water; Water-Electrolyte Balance

Differential renal function studies performed on ten patients after release of unilateral hydronephrosis revealed that the previously obstructed kidney exhibits abnormalities in a number of physiological indexes. Many of the obstructed kidneys had an impairment of glomerular filtration rate, concentrating ability, acidification, sodium reabsorption and tubular maximal secretion of para-aminohippurate with normal urinary dilution. Despite impairment of sodium and water reabsorption, none of these patients, nor 20 additional patients, had a significant postobstructive diuresis from the previously obstructed kidney. All of the patients had normal total renal function. Thus, the changes observed were a result of the obstructive injury and were not related to azotemia or aberrations in water or sodium metabolism.

Topics: Adolescent; Adult; Aminohippuric Acids; Child; Chronic Disease; Desoxycorticosterone; Diuresis; Glomerular Filtration Rate; Humans; Hydronephrosis; Inulin; Kidney; Kidney Concentrating Ability; Mannitol; Ureteral Obstruction; Vasopressins

Topics: Aged; Chronic Disease; Humans; Lung Diseases, Obstructive; Male; Respiratory Insufficiency; Respiratory Tract Infections; Vasopressins

Topics: Adrenocorticotropic Hormone; Carcinoma; Chronic Disease; Female; Hormones, Ectopic; Humans; Lung Neoplasms; Middle Aged; Thyroiditis; Vasopressins

Topics: Chronic Disease; Cyanosis; Humans; Inflammation; Lung Diseases; Male; Middle Aged; Osteoarthropathy, Secondary Hypertrophic; Penicillins; Pneumoconiosis; Smoking; Syndrome; Tetracycline; Tomography, X-Ray; Vasopressins

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

Topics: Acclimatization; Adult; Altitude; Blood Physiological Phenomena; Blood Specimen Collection; Chronic Disease; Extracellular Space; Humans; Hypoxia; Methods; Middle Aged; Osmolar Concentration; Peru; Sodium; Time Factors; Vasopressins

Topics: Acute Disease; Adult; Aged; Chronic Disease; Female; Gastrointestinal Motility; Herpes Zoster; Humans; Injections, Intramuscular; Lysine; Male; Middle Aged; Neuralgia; Osteoporosis; Pruritus; Raynaud Disease; Tabes Dorsalis; Time Factors; Trigeminal Neuralgia; Vasopressins

Topics: Adult; Aldosterone; Catecholamines; Chronic Disease; Female; Heart Failure; Humans; Male; Middle Aged; Renin; Vasopressins; Water-Electrolyte Balance

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

Topics: Acute Disease; Animals; Blood Flow Velocity; Blood Pressure; Blood Proteins; Chronic Disease; Creatinine; Dogs; Glomerular Filtration Rate; Hematocrit; In Vitro Techniques; Kidney; Natriuresis; Organ Size; Oxygenators; Perfusion; Potassium; Sodium; Vasopressins

Topics: Adenine Nucleotides; Adolescent; Adult; Aged; Chronic Disease; Circadian Rhythm; Creatinine; Cyclic AMP; Female; Glomerulonephritis; Glucagon; Growth Hormone; Humans; Hyperparathyroidism; Hypoparathyroidism; Male; Menstruation; Middle Aged; Osmolar Concentration; Parathyroid Hormone; Phosphates; Pregnancy; Pyelonephritis; Tritium; Urine; Vasopressins

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

Topics: Adolescent; Adult; Alkaline Phosphatase; Blood Urea Nitrogen; Calcinosis; Calcium; Chronic Disease; Creatinine; Female; Humans; Hyperparathyroidism; Kidney Concentrating Ability; Kidney Diseases; Kidney Tubules; Male; Middle Aged; Osmolar Concentration; Phosphorus; Potassium; Sodium; Urea; Vasopressins

Topics: Adult; Aged; Chronic Disease; Diabetes Insipidus; Female; Humans; Hypernatremia; Vasopressins

Topics: 17-Hydroxycorticosteroids; 17-Ketosteroids; Acute Disease; Adrenocorticotropic Hormone; Adult; Chronic Disease; Female; Humans; Hypothalamo-Hypophyseal System; Male; Metyrapone; Middle Aged; Multiple Sclerosis; Neurologic Manifestations; Pituitary-Adrenal Function Tests; Pituitary-Adrenal System; Stimulation, Chemical; Vasopressins

Topics: Adult; Anticonvulsants; Calcium; Chlorides; Chronic Disease; Creatinine; Epilepsy; Female; Humans; Intellectual Disability; Male; Mass Screening; Metabolic Clearance Rate; Middle Aged; Osmolar Concentration; Phenobarbital; Phenytoin; Potassium; Sodium; Specific Gravity; Time Factors; Urea; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Aged; Aldosterone; Arteriosclerosis; Blood Pressure; Blood Volume; Cardiac Output; Chronic Disease; Digitalis Glycosides; Diuretics; Electrocardiography; Female; Heart Diseases; Heart Failure; Humans; Hypertension; Kidney; Male; Middle Aged; Mitral Valve Insufficiency; Mitral Valve Stenosis; Regional Blood Flow; Serum Albumin, Radio-Iodinated; Vasopressins

Topics: Adult; Aged; Blood Pressure; Blood Volume; Chronic Disease; Female; Furosemide; Heart Failure; Humans; Kidney Function Tests; Lanatosides; Male; Middle Aged; Osmosis; Potassium; Renal Artery; Sodium; Urine; Vasopressins

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