pituitrin and Edema

Burn injury represents a significant problem worldwide. Advances in therapy strategies, based on better understanding of the pathophysiologic responses after burn injury have improved the clinical outcome of patients with burn injuries over the past years. This article describes the present understanding of the pathophysiology of a burn injury including both the local and systemic responses, focusing on the many facets of organ and systemic effects directly resulting from hypovolemia and circulating mediators following burn trauma.

Topics: Angiotensin II; Animals; Burns; Catecholamines; Edema; Hemodynamics; Histamine; Humans; Hypovolemia; Inflammation Mediators; Platelet Activating Factor; Prostaglandins; Serotonin; Skin; Soft Tissue Injuries; Thromboxanes; Vascular Resistance; Vasopressins

Oedematous malnutrition, represented by its most severe form kwashiorkor, is rampant in many parts of the world and is associated with a high case fatality rate. Despite being first described more than a century ago, the pathogenesis of kwashiorkor is still not clear. The traditional thinking is that it results from a deficiency of dietary protein and is usually associated with an infection. This has now been challenged by the finding that there is no difference in diets of children developing marasmus or kwashiorkor. Nutritional oedema is associated with an increased secretion of anti-diuretic substance (probably antidiuretic hormone) which prevents the normal excretory response to water administration. Experimental studies have shown that feeding low-protein, low-calorie diets results in delayed and incomplete response to a water load, and that the livers of the animals show a reduced capacity for inactivating anti-diuretic hormone. There is now evidence that links generation of free radicals and depletion of anti-oxidants with the development of oedema in kwashiorkor.

Topics: Aldosterone; Animals; Child; Edema; Ferritins; Humans; Kwashiorkor; Malnutrition; Models, Biological; Oxidative Stress; Protein-Energy Malnutrition; Vasopressins

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

Topics: Cushing Syndrome; Edema; Humans; Hyperaldosteronism; Hypertension; Hypokalemia; Hyponatremia; Inappropriate ADH Syndrome; Mineralocorticoid Excess Syndrome, Apparent; Renin-Angiotensin System; Vasopressins

This article discusses the pathophysiology of sodium and water retention in edematous disorders with a particular focus on cardiac failure, cirrhosis, and pregnancy. The body fluid volume hypothesis, which emphasizes the dominant role of arterial baroreceptors in renal sodium and water excretion, is reviewed. With arterial underfilling, either due to a decrease in cardiac output or peripheral arterial vasodilation, the normal central inhibition of the sympathetic nervous system activity and baroreceptor-mediated, nonosmotic arginine vasopressin (AVP) release is attenuated. The resultant increase in renal adrenergic activity stimulates the renin-angiotensin-aldosterone system. Although the resultant increase in systemic vascular resistance compensates for the primary arterial underfilling, this activation of the neurohumoral axis results in diminished sodium and water delivery to the renal collecting duct sites of aldosterone, AVP, and natriuretic peptide action. This diminished distal sodium and water delivery will be discussed as an important factor in the failure to escape from the sodium-retaining effects of aldosterone, the resistance to the natriuretic and diuretic effects of natriuretic peptides, and the diminished maximal solute-free water excretion in patients with edema. The role of the nonosmotic AVP release in water retention and hypo-osmolality/hyponatremia has been demonstrated in patients and experimental animals by administering nonpeptide, orally active vasopressin V2 receptor antagonists. These agents have been found to increase solute-free water excretion in patients with water-retaining, hyponatremic edema as well as in experimental animals.

Topics: Aldosterone; Body Water; Edema; Female; Heart Failure; Humans; Hyponatremia; Liver Cirrhosis; Pregnancy; Pregnancy Complications; Renin-Angiotensin System; Vasodilation; Vasopressins

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

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

Hyponatremia in virtually all patients results from water retention due to an inability to excrete ingested water. In most cases, this defect represents the persistent secretion of ADH (such as in effective circulating volume depletion, and in the syndrome of inappropriate ADH secretion), although free water excretion can also be limited in disorders in which ADH levels may be appropriately suppressed (such as in advanced renal failure, and in primary polydipsia). The symptoms of hyponatremia primarily reflect neurologic dysfunction induced by cerebral edema and are related both to the severity and to the rapidity of reductions in the plasma sodium concentration. The degree of cerebral edema which occurs in acute hyponatremia is much less with chronic hyponatremia, because the brain cells lose solutes, leading to the osmotic movement of water out the cells and less brain swelling. In general, hyponatremia is corrected acutely by giving Na+ to patients who are volume-depleted and by restricting water intake in patients who are normovolemic or edematous. The optimal rate of correction should be defined to prevent the risk of central demyelinating lesions.

Topics: Adrenal Insufficiency; Adult; Brain Edema; Edema; Female; Humans; Hyponatremia; Hypothyroidism; Inappropriate ADH Syndrome; Kidney Failure, Chronic; Models, Biological; Osmolar Concentration; Potassium; Pregnancy; Syndrome; Vasopressins

Topics: Animals; Aquaporin 2; Aquaporin 6; Aquaporins; Edema; Female; Fibrosis; Heart Failure; Humans; Kidney; Models, Biological; Pregnancy; Sodium; Vasodilation; Vasopressins

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

Topics: Edema; Hemodynamics; Humans; Microcirculation; Vasopressins; Water-Electrolyte Balance

Sodium and water retention is characteristic of edematous disorders including cardiac failure, cirrhosis, nephrotic syndrome and pregnancy. In recent years the use of a sensitive radioimmunoassay for plasma vasopressin has implicated the role of nonosmotic vasopressin release in the water retention of these edematous disorders. In experimental studies and studies in humans it has been found that the nonosmotic release of vasopressin is consistently associated with activation of the sympathetic nervous and renin-angiotensin-aldosterone systems. Moreover, the sympathetic nervous system has been shown to be involved in the nonosmotic release of vasopressin (carotid and aortic baroreceptors) and activation of the renin-angiotensin system (renal beta-adrenergic receptors). These findings have led to our proposal that body fluid volume regulation involves the dynamic interaction between cardiac output and peripheral arterial resistance. In this context neither total extracellular fluid (ECF) volume nor blood volume are determinants of renal sodium and water excretion. Rather, renal sodium and water retention is initiated by either a fall in cardiac output (e.g. ECF volume depletion, low-output cardiac failure, pericardial tamponade or hypovolemic nephrotic syndrome) or peripheral arterial vasodilation (e.g. high-output cardiac failure, cirrhosis, pregnancy, sepsis, arteriovenous fistulae and pharmacologic vasodilators). With a decrease in effective arterial blood volume (EABV), initiated by either a fall in cardiac output or peripheral arterial vasodilation, the acute response involves vasoconstriction mediated by angiotensin, sympathetic mediators and vasopressin. The slower response to restoring EABV involves vasopressin-mediated water retention and aldosterone-mediated sodium retention. The renal vasoconstriction which accompanies those states that decrease EABV, by either decreasing cardiac output or causing peripheral arterial vasodilation, limits the distal tubular delivery of sodium and water thus maximizing the water-retaining effect of vasopressin and impairing the normal escape from the sodium-retaining effects of aldosterone. The elevated glomerular filtration rate and filtered sodium load in pregnancy allows increased distal sodium and water delivery in spite of a decrease in EABV, thus limiting edema formation during gestation.

Topics: Blood Volume; Cardiac Output; Cardiac Output, Low; Edema; Female; Fibrosis; Humans; Kidney; Natriuresis; Nephrotic Syndrome; Pre-Eclampsia; Pregnancy; Renin-Angiotensin System; Sympathetic Nervous System; Vascular Resistance; Vasodilation; Vasopressins

Edema is a collection of fluid within the body's interstitial space which occurs when there is an alteration of the Starling forces which control transfer of fluid from the vascular compartment to surrounding tissue spaces. Generalized edema results when altered Starling forces affect all capillary beds, such as occurs in cardiac failure, cirrhosis, and nephrotic syndrome. Common to these conditions is the development of increased total body sodium and water content. The kidneys play an essential role in the retention of this sodium and water. In this article we shall discuss the signals the kidneys receive for sodium and water retention in these edematous disorders (afferent mechanisms). We shall also examine the means by which the kidney responds to these signals and retains sodium and water (efferent mechanisms). As shall become apparent these edematous states may share many of the same afferent and efferent mechanisms for sodium and water retention.

Topics: Blood Volume; Body Water; Cardiac Output; Edema; Glomerular Filtration Rate; Heart Failure; Humans; Kidney; Liver Cirrhosis; Nephrotic Syndrome; Renal Circulation; Renin-Angiotensin System; Sodium; Vasopressins

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

Topics: Addison Disease; Ascites; Edema; Extracellular Space; Heart Failure; Humans; Hyponatremia; Intestinal Secretions; Kidney Failure, Chronic; Liver Cirrhosis; Potassium; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Aldosterone; Angiotensin II; Edema; Extracellular Space; Female; Glomerular Filtration Rate; Humans; Hyperaldosteronism; Hypertension; Hypotension; Juxtaglomerular Apparatus; Kidney; Kidney Diseases; Kidney Failure, Chronic; Natriuresis; Potassium; Pregnancy; Pregnancy Complications; Pressoreceptors; Regional Blood Flow; Renal Artery Obstruction; Renin; Vasopressins

Topics: Birth Weight; Body Fluids; Edema; Estrogens; Humans; Hypoproteinemia; Infant, Newborn; Infant, Premature, Diseases; Sclerema Neonatorum; Syndrome; Vasopressins; Water-Electrolyte Balance

Topics: Adrenal Cortex Hormones; Animals; Biopsy; Body Weight; Diet, Sodium-Restricted; Eclampsia; Edema; Female; Glomerulonephritis; Humans; Hypertension; Hypertension, Renal; Kidney; Kidney Diseases; Nephritis; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Pyelonephritis; Sodium; Uric Acid; Vasopressins; Water-Electrolyte Balance

Topics: Adrenal Glands; Aldosterone; Diagnosis, Differential; Edema; Extracellular Space; Female; Heart Diseases; Humans; Kidney; Kidney Diseases; Liver Cirrhosis; Male; Parasitic Diseases; Pituitary Gland; Posture; Pre-Eclampsia; Pregnancy; Pulmonary Edema; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Central Nervous System Diseases; Child; Edema; Endocrine System Diseases; Humans; Hyponatremia; Hypopituitarism; Lung Diseases; Male; Middle Aged; Neoplasms; Vasopressins

Topics: Adrenal Glands; Adrenal Medulla; Edema; Endocrine Glands; Heart; Heart Failure; Humans; Hyperaldosteronism; Shock; Thyroxine; Vasopressins

Topics: Adrenal Cortex Hormones; Aldosterone; Ascites; Diet Therapy; Edema; Humans; Liver Cirrhosis; Lymphatic System; Proteins; Vasopressins; Water-Electrolyte Balance

Topics: Aldosterone; Digitalis; Digitalis Glycosides; Diuretics; Edema; Electrolytes; Heart Failure; Hypokalemia; Physiology; Potassium; Sodium; Toxicology; Vasopressins

Topics: Alcohols; Body Water; Central Nervous System Diseases; Child; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diuresis; Edema; Ethanol; Histiocytosis, Langerhans-Cell; Homeostasis; Humans; Hyponatremia; Infant; Infant, Newborn; Kidney Diseases; Nicotine; Physiology; Pituitary Gland; Pituitary Gland, Posterior; Potassium Deficiency; Prednisone; Pyloric Stenosis; Vasopressins; Water

1. The effects of intravenous chlorthiazid and frusemide on urinary osmolality were compared in 19 hyponatraemic oedematous patients. 2. Frusemide (1 mg/kg) caused production of a dilute urine (urine/plasma osmolality ratio, Uosm./Posm., 1.64-0.84, P less than 0.01) whereas chlorthiazid (10 mg/Kg) did not (Uosm./Posm, 1.54-1.34, not significant. 3. The Osmolar clearance (Cosm.) was higher after frusemide than after chlorthiazid (11.45 vs 4.99 ml/min, P less than 0.01). When the doses of frusemide (0.25-0.5 mg/Kg) and chlorthiazid (20 mg/Kg) were chosen to give a similar Cosm. (7.25 vs 7.48 ml/min, not significant), the Uosm./Posm. was still lower after frusemide (2.20-1.00, P less than 0.001) than after chlorthiazid (1.75-1.26, P less than 0.01). 4. Exogenous vasopressin did not increase the low Uosm./Posm. after frusemide (1.00-1.00, not significant) but increased the ratio after chlorthiazid (1.34-1.68, p less than 0.01). 5. These results indicate that frusemide, but not chlorthiazid, lead to the excretion of a dilute urine in hyponatraemic oedematous patients. This dilution is not due to a greater solution excretion but is associated with a resistance to the action of vasopressin.

Topics: Adult; Chlorothiazide; Edema; Furosemide; Humans; Hyponatremia; Middle Aged; Osmolar Concentration; Vasopressins

The activity of demeclotetracyclin, and ADH antagonist, is studied in 11 ethylic patients with cirrhosis of the liver, under a large hydric diet (1500 cm3). The prescription of the cyclin (600 mg daily) is always determined by a fall of the urinary osmolarity (-36%) and by a dramatic improvement of the free water clearance (+ 60%); consecutively, we observe an increase of natremia in 8 out of 9 cases. Associated with Spironolactone (200 mg daily) the anti-ADH activity persists (the free water clearance becomes positive in 5 out of 10 patients), in spite of the natriuretic activity of anti-aldosterone ; a minimal fall of the natremia is observed in only 2 cases. The indication of Demeclotetracyclin in the curative or preventive treatment of the hyponatremia of the liver cirrhosis is discussed.

Topics: Adult; Aged; Ascites; Clinical Trials as Topic; Demeclocycline; Drug Therapy, Combination; Edema; Female; Humans; Hyponatremia; Liver Cirrhosis; Male; Middle Aged; Natriuresis; Spironolactone; Vasopressins

Topics: Aged, 80 and over; Autoantibodies; Diagnosis, Differential; Edema; Humans; Male; Multiple Myeloma; Syndrome; Synovitis; Vasopressins

Thiazolidinediones are highly beneficial in the treatment of type II diabetes. However, they are also associated with edema and increased risk of congestive heart failure. Several studies demonstrated that rosiglitazone (RGZ) increases the abundance of aquaporin-2 (AQP2) at the plasma membrane of renal cells. The aim of this study was to investigate whether RGZ might activate a transduction pathway facilitating AQP2 membrane accumulation in renal cells.. We analyzed the effect of RGZ on renal AQP2 intracellular trafficking in MCD4 renal cells by confocal microscopy and apical surface biotinylation. Cytosolic Ca(2+) dynamics were measured by a video-imaging approach in single cell. Transient Receptor Potential (TRP) channels expression was determined by RT-PCR.. We showed that in MCD4 cells, short-term exposure to RGZ dramatically increases the amount of apically expressed AQP2 independently on cAMP production, PKA activation and AQP2 phosphorylation. RGZ elicited a cytosolic Ca(2+) transient due to Ca(2+) influx prevented by ruthenium red, suggesting the involvement of TRP plasma membrane channels. We identified TRPV6 as the possible candidate mediating this effect.. Taken together these results provide a possible molecular mechanism explaining the increased AQP2 membrane expression under RGZ treatment: in renal cells RGZ elicits Ca(2+) transients facilitating AQP2 exposure at the apical plasma membrane, thus increasing collecting duct water permeability. Importantly, this effect suggests an unexplored application of RGZ in the treatment of pathological states characterized by impaired AQP2 trafficking at the plasma membrane.

Topics: Aquaporin 2; Calcium Channels; Calcium Signaling; Cell Line; Cell Membrane; Cyclic AMP; Edema; Endocytosis; Epithelial Cells; Gene Expression; Heart Failure; Humans; Kidney; Rosiglitazone; Signal Transduction; Thiazolidinediones; TRPV Cation Channels; Vasopressins

From histopathological specimens, endolymphatic hydrops has been demonstrated in association with inner ear disorders. Recent studies have observed findings suggestive of hydrops using MRI in humans. Previous studies suggest that vasopressin may play a critical role in endolymph homeostasis and may be involved in the development of Ménière's disease. In this study we evaluate the effect of vasopressin administration in vivo in longitudinal studies using two mouse strains. High resolution MRI at 9.4 T in combination with intraperitoneally delivered Gadolinium contrast, was performed before and after chronic subcutaneous administration of vasopressin via mini-osmotic pumps in the same mouse. A development of endolymphatic hydrops over time could be demonstrated in C57BL6 mice (5 mice, 2 and 4 weeks of administration) as well as in CBA/J mice (4 mice, 2 weeks of administration; 6 mice, 3 and 4 weeks of administration). In most C57BL6 mice hydrops developed first after more than 2 weeks while CBA/J mice had an earlier response. These results may suggest an in vivo model for studying endolymphatic hydrops and corroborates the future use of MRI as a tool in the diagnosis and treatment of inner ear diseases, such as Ménière's disease. MRI may also be developed as a critical tool in evaluating inner ear homeostasis in genetically modified mice, to augment the understanding of human disease.

Topics: Animals; Contrast Media; Disease Models, Animal; Ear, Inner; Edema; Endolymphatic Hydrops; Female; Gadolinium; Homeostasis; Infusions, Parenteral; Magnetic Resonance Imaging; Mice; Mice, Inbred C57BL; Mice, Inbred CBA; Osmosis; Vasopressins

To evaluate the relationship between leg edema, nocturnal urine volume (NUV), and the secretion of antidiuretic hormone (ADH) during the night, and to investigate the principal factors affecting nocturnal polyuria in older men.. A total of 74 male inpatients more than 50 years of age were enrolled in this study. Blood count, standard chemistry panel, brain natriuretic peptide (BNP), urinary ADH (u-ADH), urinary creatinine (u-Cre), and urinary osmolarity were measured at 6:00 am. Keeping a frequency volume chart, bioelectric impedance analysis was performed at 5 pm. Leg edema was measured as an edema ratio, using the following formula: extracellular water [L)/(extracellular water [L) + intracellular water [L)) in legs.. A total of 66 patients were evaluated. NUV had a significant positive correlation with leg edema (r = 0.32, P = .008), negative correlation with u-ADH/u-Cre (r = -0.37, P = .003) but not BNP. Leg edema had a significant positive correlation with the level of BNP (r = 0.33, P = .012) and negative correlation with u-ADH/u-Cre (r = -0.4, P = .001). However a partial correlation showed that there was no significant correlation between NUV and leg edema. A multivariate logistic model showed that only u-ADH/u-Cre was an independent predictive variable of nocturnal polyuria.. This study suggested that leg edema influenced nocturnal urine volume with an associated decrease in ADH secretion but not directly. ADH secretion during the night was the principal factor affecting NP in older men.

Topics: Aged; Blood Pressure; Edema; Heart Failure; Humans; Leg; Male; Middle Aged; Natriuretic Peptide, Brain; Nocturia; Osmolar Concentration; Polyuria; Vasopressins

A 61-year-old man had hyponatremia (serum Na 112 mmol/L), which was associated with disturbance of consciousness. Therefore, administration of hypertonic saline was commenced. Eventually he was diagnosed with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Hypertonic saline was continued for 45 days, and plasma Na concentration rose to 138 mmol/L. At that time we were consulted regarding further administration of hypertonic saline. At the time of the consultation marked edema had developed affecting the whole body. The cardiothoracic ratio was increased and pleural effusion was evident on the chest X-ray. Administration of hypertonic saline was discontinued to prevent further worsening of the edema. Furthermore, water restriction (500 mL/day) was started. Body weight decreased by 4.3 kg in 7 days and the edema was diminished. However, plasma Na concentration decreased to 117 mmol/L. At that stage, we needed to balance the treatment of hyponatremia to the increased extracellular fluid volume (ECF). To normalize the ECF, we carried out ultrafiltration (UF) three times. Resolution of edema by using an extracorporeal UF method allowed the control of plasma Na concentration. In this case increased ECF volume hindered the adjustment of plasma Na concentration. The infusion of hypertonic saline is now used commonly by physicians. It is necessary to consider the potential risks of such treatment.

Topics: Edema; Esthesioneuroblastoma, Olfactory; Humans; Inappropriate ADH Syndrome; Magnetic Resonance Imaging; Male; Middle Aged; Nasal Cavity; Nose Neoplasms; Pleural Effusion; Radiography; Saline Solution, Hypertonic; Sodium; Ultrafiltration; Vasopressins

Recently, there has been a growing interest in long-term consequences of neonatal pain because modern neonatal intensive care units routinely employ procedures that cause considerable pain and may be followed by local inflammation and hyperalgesia lasting for several hours or even days. To address this question, we developed a rat model of short lasting (<2 days) early local inflammatory insult produced by a single injection of 0.25% carrageenan (CAR) into the plantar surface of a hindpaw. Previously, we demonstrated that rats receiving this treatment within the first week after birth grow into adults with a global reduction in responsiveness to acute pain. Here, we report that these animals also manifest a low anxiety trait associated with reduced emotional responsiveness to stress. This conclusion is based in the following observations: (a) rats in our model display reduced anxiety on an elevated plus-maze; (b) in the forced swim test, these rats exhibit behavioral characteristics associated with stronger ability for stress coping; and (c) these animals have reduced basal and stress-induced plasma levels of such stress-related neuroendocrine markers as corticotropin-releasing factor, vasopressin, and adrenocorticotrophic hormone. In addition, we used DNA microarray and real-time reverse-transcriptase polymerase chain reaction to profile long-term changes in gene expression in the midbrain periaqueductal gray (PAG; a region involved in both stress and pain modulation) in our animal model. Among the affected genes, serotonergic receptors were particularly well represented. Specifically, we detected increase in the expression of 5-HT1A, 5-HT1D, 5-HT2A, 5-HT2C and 5-HT4 receptors. Several of these receptors are known to be involved in the anxiolytic and analgesic activity of the PAG. Finally, to determine whether neonatal inflammatory insult induces elevation in maternal care, which may play a role in generating long-term behavioral alterations seen in our model, we examined maternal behavior for 3 days following CAR injection. Indeed, we observed a substantial increase in maternal attention to the pups at the time of inflammation, but this increase was not without its cost: a period of significant maternal neglect afterward.

Topics: Adrenocorticotropic Hormone; Analysis of Variance; Animals; Animals, Newborn; Behavior, Animal; Brain Chemistry; Carrageenan; Carrier Proteins; Corticotropin-Releasing Hormone; Disease Models, Animal; Edema; Enzyme-Linked Immunosorbent Assay; Female; Inflammation; Male; Maternal Behavior; Maze Learning; Oligonucleotide Array Sequence Analysis; Pain; Pain Measurement; Periaqueductal Gray; Phosphoproteins; Rats; Receptors, Serotonin; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Stress, Psychological; Swimming; Time Factors; Vasopressins

Yamanouchi is developing conivaptan, a diuretic and active vasopressin V1a and V2 antagonist, which has an aquaretic effect, for the potential treatment of hyponatremia and heart failure. In January 2004, Yamanouchi submitted an NDA in the US for injectable conivaptan for the treatment of hyponatremia and, in December 2004, the FDA issued approval, although additional safety data were requested.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Clinical Trials as Topic; Clinical Trials, Phase III as Topic; Diuretics; Edema; Heart Failure; Humans; Hyponatremia; Molecular Structure; Structure-Activity Relationship; Vasopressins

Topics: Edema; Fluid Therapy; Hospitalization; Humans; Hypernatremia; Saline Solution, Hypertonic; Vasopressins; Water-Electrolyte Balance

Antidiuretic actions induced by two growth hormone (GH) isoforms (20 K- and 22 K-hGH; 0.2 and 2.0 mg/kg) were evaluated in rats, as fluid retention may cause oedema, one of the adverse effects of GH. Both GH isoforms (2.0 mg/kg) suppressed urine excretion in hypophysectomized rats (P< 0.01), but only the 22 K-hGH isoform (2.0 mg/kg) suppressed urine excretion in intact rats (P< 0.01). In addition, prolactin (PRL) suppressed urine excretion in intact rats (P< 0.05). In conclusion, 20 K-hGH has less potency in causing urine retention than 22 K-hGH and since 20 K-hGH is missing 15 amino acids found in 22 K-hGH, these amino acids may be important for the antidiuretic action of GH. Since prolactin suppressed urine excretion, a part of the antidiuretic action of GH may be related to PRL-R activation.

Topics: Animals; Body Weight; Diuresis; Edema; Growth; Human Growth Hormone; Humans; Hypophysectomy; Male; Molecular Weight; Pituitary Gland; Prolactin; Rats; Rats, Sprague-Dawley; Recombinant Proteins; Vasopressins; Water-Electrolyte Balance

32 out of 83 in patients with atopic dermatitis showed a decrease of urine excretion during acute exacerbation and elevated levels of antidiuretic hormone (ADH 23 of 29 cases), renin (18 of 32 cases), angiotensin (22 of 29 cases) and aldosterone (16 of 37 cases). Six cases with high ADH showed severe pitting edema of lower legs with hypoalbuminemia. ADH, volume of urine and edema were improved when their skin symptoms subsided. There was no statistically significant relationship between the dose of steroid ointment and ADH. Also there was no correlation between low 17-OHCS or 17-KS and high ADH or renin.

Topics: Adult; Aldosterone; Angiotensin I; Dermatitis, Atopic; Edema; Female; Humans; Male; Renin; Vasopressins

To study the regulation of antidiuretic hormone (ADH) and atrial natriuretic peptide (ANP) in obese and lean women with a swelling syndrome.. Thirty-four obese women and 12 lean women with a swelling syndrome and an abnormal isotopic test of capillary permeability to albumin were investigated.. After 10 nocturnal hours of fluid restriction, subjects were asked at 8am to ingest a tap water load of 20 ml/kg within 10 min and to remain strictly recumbent until twelve noon on the first day, and to remain standing and to walk around until twelve noon on the second day. Free water clearance and the cGMP/creatinine and albumin/creatinine ratios were determined hourly in the morning.. The total 4 h-urinary volume/ingested water volume ratio was significantly lower on the second day both in the lean and the obese patients, the differences being slightly larger in the obese patients. The increase in free water clearance was significantly less on the second day in the obese patients. The increase in cGMP/creatinine ratio was also significantly lower on the second day in the obese patients. The maximum level of the urinary albumin/creatinine ratio was significantly higher on the second day in the obese patients.. In obese women with a swelling syndrome: (1) The higher increase in the urinary albumin excretion rate after water loading followed by a sustained upright position suggests a widespread alteration in capillary function, which is also indicated by the isotopic test of capillary permeability to albumin. (2) The water load-induced inhibition of ADH secretion and stimulation of ANP secretion or ANP activity, more defective in the upright position than in the recumbent one, is probably another major contributing factor to orthostatic oedema.

Topics: Adult; Albumins; Atrial Natriuretic Factor; Capillary Permeability; Case-Control Studies; Creatinine; Drinking; Edema; Female; Guanosine Monophosphate; Humans; Middle Aged; Obesity; Posture; Statistics, Nonparametric; Vasopressins

Plasma antidiuretic hormone (p-ADH) concentrations were determined with a radioimmunoassay, using a reversed-phase C18 silica column, in 300 patients with vertigo, dizziness and/or deafness; 119 of them had a diagnosis of Menière's disease. The p-ADH level was significantly elevated in patients with Meniere's disease and others with endolymphatic hydrops, e.g. cochlear Menière's disease or delayed hydrops. By contrast, the p-ADH level was not so high in cases without the endolymphatic hydrops. The increase in the p-ADH level was closely linked to vertigo attacks, the glycerol test results and an enhanced negative summating potential (-SP) in electrocochleogram (ECochG). These results lead to the assumption that disorders of ADH-dependent hormonal control in the inner ear may constitute the possible mechanism underlying vertiginous attacks and deafness in patients with endolymphatic hydrops.

Topics: Cochlea; Deafness; Dizziness; Edema; Electrophysiology; Endolymphatic Hydrops; Glycerol; Heating; Humans; Meniere Disease; Vasopressins; Vertigo

The effect of dextroamphetamine sulfate (Dexedrine) on plasma opioid peptides, hormones, and other metabolites was studied in eight female subjects with idiopathic (orthostatic) edema and five healthy females. All subjects were given 20 mg of dextroamphetamine sulfate, a drug widely used in the treatment of this disorder, and blood samples were collected before and 30, 60, and 90 minutes after treatment. Patients with idiopathic (orthostatic) edema had significantly lower plasma sodium levels but higher blood urea nitrogen, aldosterone, and renin levels. D-amphetamine decreased aldosterone and renin levels in both groups. Plasma adrenocorticotropin levels were lower whereas met-enkephalin levels were higher in idiopathic (orthostatic) edema subjects compared to control subjects. D-amphetamine had no significant effect on plasma beta-endorphin, adrenocorticotrophic hormone, or enkephalins. Our data indicate that opioid peptides, especially enkephalins, and adrenocorticotrophic hormone may be involved in the pathogenesis of idiopathic (orthostatic) edema syndrome, but they seem uninvolved in the aldosterone- and renin-lowering action of amphetamine. It is possible that amphetamine is acting further down the chain, either directly on the adrenal and kidney or the microvasculature, rather than at hypothalamus-pituitary axis.

Topics: Adrenocorticotropic Hormone; Adult; Aldosterone; beta-Endorphin; Blood Urea Nitrogen; Body Weight; Dextroamphetamine; Dopamine; Edema; Endorphins; Enkephalin, Leucine; Enkephalin, Methionine; Female; Humans; Hypotension, Orthostatic; Middle Aged; Renin; Sodium; Spironolactone; Syndrome; Vasopressins

As many as 26 children (20 boys and 6 girls) aged 2.5 to 15.5 years suffering from active nephrotic glomerulonephritis were examined for the intravascular liquid volume and antidiuretic hormone in blood plasma. In accordance with the magnitude of the circulating blood volume, 3 groups of patients were distinguished: group I included patients with hypervolemia, group II with hypovolemia, and group III with normovolemia. In the hypovolemic children, the nephrotic syndrome occurred at an earlier age as compared to the normovolemic children who developed it much later. The patients differed in the content of antidiuretic hormone and total blood protein. In the second group children, secretion of antidiuretic hormone was the highest one, whereas the level of total protein was the least one. A relationship was discovered between the pattern of the nephrotic syndrome and the efficacy of diuretic treatment.

Topics: Adolescent; Age Factors; Blood Proteins; Blood Volume; Child; Child, Preschool; Edema; Female; Humans; Male; Nephrosis, Lipoid; Osmolar Concentration; Vasopressins

SK&F 101926, a synthetic peptide, is a potent antagonist of vasopressin at both the V2 and the V1 receptors. Following intravenous administration of SK&F 101926 (5 mg/kg), mean arterial pressure (MAP) immediately fell 75 mm Hg. Heart rate increased approximately 50 beats/min. Cutaneous flushing and cyanosis appeared approximately 2 to 5 min after the SK&F 101926 administration. Three of the five rats died within 40 min with no improvement in either color or MAP. The two surviving animals slowly recovered from these symptoms. The hypotension and flushing recorded in these studies resembled the effects during hypotensive shock. SK&F 101926 degranulated rat peritoneal mast cells in vitro as measured by the liberation of histamine. Analogs of SK&F 101926 were identified having reduced activity to release histamine from mast cells in vitro. The activity of these analogs to release histamine in vivo was also tested, as reflected by rat paw edema. A positive correlation was found between the potency to produce edema in vivo and the potency to release mast cell histamine in vitro (r = 0.94, p less than 0.05). In addition, compounds that released mast cell histamine and induced rat paw edema also produced hypotension and death when administered intravenously, while analogs which produced minimal histamine release in vitro produced minimal or no cardiovascular changes or lethality in vivo at the same dosages (5 mg/kg). Finally, cyproheptadine (10 mg/kg), an antagonist at both the serotonin and the histamine receptors, blunted the effects of SK&F 101926 on MAP and blocked the lethality. Pretreatment with a combination of histamine (H1 and H2) antagonists provided little protection against the SK&F 101926-induced toxicity. These data indicate that the cardiovascular toxicity of SK&F 101926 (and related peptides) is mediated via the release of autocoids from mast cells. Serotonin appears to play a major role in mediating the cardiovascular toxicity of SK&F 101926.

Topics: Animals; Arginine Vasopressin; Cell Degranulation; Edema; Hindlimb; Histamine Release; Hypotension; Male; Mast Cells; Rats; Rats, Inbred Strains; Time Factors; Vasopressins

Ingestion of licorice, 100 g daily for 8 weeks, caused a rise in 81% in plasma atrial natriuretic peptide (ANP) concentration in 12 healthy subjects. Mean body weight increment (1.6 kg) correlated with the increase in plasma ANP (r = 0.59; P less than 0.01). The plasma concentrations of antidiuretic hormone, aldosterone, and plasma renin activity decreased. All these hormonal effects, reflecting retention of sodium and fluid volume, were probably due to the known mineralocorticoid properties of licorice. Blood pressure increased transiently and two subjects developed reversible hypertension. The rise in plasma ANP concentration during ingestion of licorice may be considered a physiological response to prevent fluid retention and development of hypertension.

Topics: Adult; Atrial Natriuretic Factor; Blood Pressure; Edema; Female; Glycyrrhiza; Humans; Male; Middle Aged; Plants, Medicinal; Renin-Angiotensin System; Time Factors; Vasopressins

Local intra-arterial infusions of histamine, 16 micrograms base/min, for 60 minutes produced increases in lymph flow, lymph total protein concentration, the lymph/plasma total protein ratio, and weight in canine forelimbs perfused at constant flow. The weight gains were far greater than can be accounted for by an increase in vascular volume, and must, therefore, be attributed to edema formation. Treatment with dopamine (2, 4, or 8 micrograms base/min) or arginine vasopressin (AVP) initially produced an increase in perfusion pressure reflecting constriction of the forelimb vasculature. AVP prevented the histamine-induced increase in lymph flow, lymph total protein concentration, the L/P total protein ratio, and weight gain. In contrast, treatment with DA at three different dose levels failed to affect the histamine response. The increases in lymph flow, lymph total protein concentration, lymph/plasma total protein ratio, and weight were comparable to that produced by histamine in the absence of DA. These data fail to provide evidence for DA mediated regulation of macromolecular permeability, and suggest that endothelial cells either do not contain DA receptors, or that their activation does not affect macromolecular permeability.

Topics: Animals; Cell Membrane Permeability; Dogs; Dopamine; Edema; Female; Forelimb; Histamine; Infusions, Intra-Arterial; Lymph; Macromolecular Substances; Male; Organ Size; Vasopressins; Venous Pressure

Topics: Aldosterone; Blood Proteins; Edema; Edema, Cardiac; Extracellular Space; Glomerular Filtration Rate; Humans; Liver Cirrhosis; Natriuretic Agents; Nephritis; Obesity; Proteins; Vasopressins; Water-Electrolyte Balance

Decreased free water excretion and the development of interstitial edema are recognized characteristics of preeclampsia. However, the pathophysiology of decreased urine excretion in preeclampsia is presently controversial: diminished glomerular filtration, renal arteriolar spasm, elevated plasma vasopressin levels, and plasma volume contraction have been suggested as etiologies. We studied seven pregnant patients with a diagnosis of mild preeclampsia to assess the role of vasopressin, serum protein, and glomerular function in the renal excretion of water. The ability to excrete a water load was significantly and directly correlated with serum albumin (P less than 0.05) and protein (P less than 0.02) concentrations. Neither plasma vasopressin nor creatinine clearance correlated with water excretion. The similarity of preeclampsia and the nephrotic syndrome with regard to the renal excretion of water is discussed.

Topics: Anuria; Edema; Female; Glomerular Filtration Rate; Humans; Nephrotic Syndrome; Oliguria; Pre-Eclampsia; Pregnancy; Vasopressins; Water

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

In order to investigate the role of ADH and the renal handling of sodium and water in patients with idiopathic edema, 21 patients were subjected to acute oral water load tests. Although a normal water diuresis was observed in al patients in supine posture, it was markedly impaired in upright posture with significant decreases in sodium, free water, and osmolar clearances. In particular, two patients exhibited the continuous production of concentrated urine after the water load in upright posture. The fractional reabsorption of sodium at the proximal tubules was significantly increased in upright posture, while the glomerular filtration rate did not change significantly. The constricting of both legs with elastic bandages tended to improve the water diuresis in upright posture, suggesting that the pooling of blood into the lower legs might be contributing to the formation of idiopathic edema. The patients showed normal osmoregulation of ADH release in supine, but not in upright posture: the suppression of ADH release in upright posture was only transient or incomplete despite a sufficient fall in plasma osmolality following the water load. Thus, both an increase in renal sodium reabsorption and the insufficient suppression of ADH release in upright posture might contribute to the retention of body fluid in patients with idiopathic edema.

Topics: Adolescent; Adult; Blood Volume; Body Water; Edema; Female; Glomerular Filtration Rate; Humans; Kidney; Osmolar Concentration; Posture; Sodium; Vasopressins

In dogs anesthetized with pentobarbital, 60 min local i.a. infusions of prostaglandin E1 (4 micrograms/min) together with bradykinin (10 micrograms base/min) into forelimbs perfused at a constant pump controlled flow rate produced decreases in perfusion pressure and very marked increases in lymph flow, lymph total protein concentration, total protein transport and weight (266 g). Pretreatment with indomethacin did not significantly reduce the very marked increases in these parameters produced by the combined prostaglandin E1-bradykinin infusions. Treatment with diphenhydramine completely prevented the increases in lymph flow, lymph total protein concentration, total protein transport, weight and vasodilation produced by infusions of histamine, but not those produced by infusions of prostaglandin E1 or bradykinin. Pretreatment with methylprednisolone prevented the increases in lymph flow, lymph total protein concentration, total protein transport and weight produced by infusions of prostaglandin E1, but not those produced by infusions of high doses of histamine or bradykinin. Treatment with either methylprednisolone or diphenhydramine significantly reduced the very marked increases in these parameters produced by combined infusions of prostaglandin E1 and bradykinin to levels produced by infusions of bradykinin alone. Vasopressin or isoproterenol treatment essentially prevented the very marked increases in lymph flow, lymph total protein concentration, total protein transport and weight produced by combined infusions of prostaglandin E1 and bradykinin. These data suggest that the potentiation of the bradykinin edema formation produced by prostaglandin E1 results from an endogenous release of histamine and that treatment with vasopressin or isoproterenol essentially prevents the development of edema produced by combined infusions of these autacoids. Moreover, the potentiation is not dependent on the vasodilator action of prostaglandin E1 as it may be demonstrated under constant controlled flow conditions.

Topics: Alprostadil; Animals; Bradykinin; Diphenhydramine; Dogs; Drug Synergism; Edema; Female; Forelimb; Histamine Release; Indomethacin; Infusions, Intra-Arterial; Isoproterenol; Male; Methylprednisolone; Prostaglandins E; Vasodilation; Vasopressins

In several animal species, constriction of the thoracic inferior vena cava (TIVCC) is known to increase proximal sodium reabsorption and inhibit natriuresis following saline loading, leading to edema. To eluicidate the role of adrenal and hypophyseal hormones in the development of edema, kidney and liver functions after TIVCC were compared in adrenalectomised or hypophysectomised rats, and in intact controls. It was found that edema (body weight increase) and kidney and liver affliction were much less pronounced after the operations. The roles of aldosterone and ADH deficiency in renal sodium and water excretion are discussed. It is concluded that adrenal and hypophyseal hormones do not initiate edema but modulate its extent. The absence of edematous changes in the liver of hypophysectomised and adrenalectomised rats deserves further attention.

Topics: Adenosine Triphosphatases; Adrenalectomy; Animals; Constriction; Edema; Glomerular Filtration Rate; Hypophysectomy; Kidney; Liver; Male; Potassium; Rats; Sodium; Succinate Dehydrogenase; Vasopressins; Vena Cava, Inferior

Topics: Acute Kidney Injury; Adult; Blood Pressure; Blood Volume; Brain Edema; Chemoreceptor Cells; Edema; Female; Humans; Kidney; Kidney Concentrating Ability; Kidney Failure, Chronic; Male; Pressoreceptors; Renin-Angiotensin System; Vasopressins; Water-Electrolyte Balance

In the isolated perfused hind legs of rats with enemas induced by carrageenin, dextran or Freund's adjuvant in both paws, resting perfusion pressure was slightly increased whereas the vasopressor action of noradrenaline, lysine-vasopressin and prostaglandin F2 alpha, was decreased. Admixture of indomethacin (3 micrograms.ml-1) to the perfusion fluid led to a decrease of resting perfusion pressure whereas its influence on EAmax of noradrenaline was only weak under these conditions. Concomitantly, the contents of prostaglandin E-like substances in the perfusate decreased. Prostaglandin F2 alpha exhibits only weak vasopressor activity in isolated perfused hind legs of rats with carrageenin edema. Altogether, the effect of indomethacin on resting perfusion pressure as well as on EA and EAmax, resp., of agonists is difficulty to explain by its effect on arachidonic acid cascade. The pD2-value of noradrenaline (4.68 - 4.87) and lysine-vasopressin (6.02 - 6.04) was apparently not changed, at least not decreased, in the acute phase of inflammation indicating no impairment of receptor affinity of noradrenaline and vasopressin in inflammation. Blood vessel reaction is apparently influenced in inflammation mechanically by the increased tissue pressure as well as by molecular mechanisms consisting in the presence of inflammatory mediators and/or particularly in a reduced intrinsic sensitivity of the blood vessel muscle itself.

Topics: Animals; Arthritis; Arthritis, Experimental; Blood Vessels; Dinoprost; Edema; Female; Hindlimb; In Vitro Techniques; Indomethacin; Norepinephrine; Perfusion; Prostaglandins F; Rats; Rats, Inbred Strains; Vasopressins

In advanced heart failure, severe edema develops associated with hyponatremia. In 20 patients with severe congestive heart failure, we studied plasma antidiuretic hormone (ADH) concentrations related to hemodynamics and plasma osmolality. Prazosin was used to test the acute response to changes in atrial receptors and hemofiltration to test the response to changes in volume receptors. One group of the patients had inappropriately high ADH values (14.5 +/- 8.8 pg/ml) in relation to their plasma osmolality, which was well below normal values (276 +/- 23 mosmol/kg water) with no apparent osmoregulatory control. The other group showed a normal relationship of ADH and plasma osmolality (3.9 +/- 1.0 pg/ml; 289 +/- 8 mosmol/kg water), Only in the normal regulating group did lowering of left atrium pressure by prazosin result in a rise in ADH related to the decrease in pressure. Inappropriately high ADH secretion could be reversed by hemofiltration. This suggests that the syndrome of "dilutional hypo-osmolality" in severe congestive heart failure may be caused by an inappropriately high ADH secretion in which the osmoreceptor system is dominated by nonosmolar stimuli; however, it cannot be ruled out that associated hemodynamic effects in the kidney or other intrarenal or hormonal factors contribute to this mechanism.

Topics: Adult; Edema; Heart Failure; Hemodynamics; Humans; Hyponatremia; Middle Aged; Osmolar Concentration; Prazosin; Vasopressins

Topics: Diagnosis, Differential; Edema; Humans; Hyponatremia; Vasopressins; Water; Water-Electrolyte Balance

In order to investigate the etiology of idiopathic edema, clinical findings and endocrinological abnormalities were analyzed in twenty-seven patients, and the following results were obtained. An easy occurrence of subcutaneous bleeding and positive Rumpel-Leede phenomenon were observed in the majority of the patients. ADH, plasma renin activity and plasma aldosterone concentration in the patients did not show abnormalities following water loading in the supine position when compared with normal controls. But the results obtained in the present study suggested that they might contribute to water and sodium retention in the upright position. In the patients, plasma prolactin levels were not decreased, but rather increased and urinary excretion of kallikrein and kinin was reduced significantly after water loading in the upright position. Thus, prolactin and urinary kallikrein-kinin system might also contribute to water and sodium retention in idiopathic edema, directly or indirectly through the augmentation of the action of ADH and of aldosterone. It was concluded that the increased vascular permeability and endocrinological polyfactors play a role, in a cooperative fashion, in the mechanism of this disease.

Topics: Adult; Aldosterone; Blood Volume; Body Water; Capillary Permeability; Edema; Female; Hematocrit; Humans; Kallikreins; Kinins; Male; Middle Aged; Posture; Prolactin; Renin; Urination; Vasopressins

Topics: Anuria; Diabetes Insipidus; Edema; Humans; Inappropriate ADH Syndrome; Oliguria; Syndrome; Vasopressins; Water-Electrolyte Balance

The renal response to left atrial balloon inflation in normal dogs was compared with that in dogs with chronic congestive heart failure (CHF). CHF was induced by the production of an aortocaval fistula below the level of the renal arteries. CHF dogs showed elevated left ventricular end-diastolic pressure, enlarged hearts, a depression of myocardial contractility, pulmonary edema, ascites, and peripheral edema. They also showed significant decreases in urine flow, creatinine clearance, para-aminohippurate clearance, sodium and potassium excretion, fractional sodium excretion, osmolar clearance, arterial blood pressure, and heart rate. Balloon distension of the left atrium evoked a significant increase in urine flow and free-water clearance in the normal group. The reflex nature of this response was indicated by its blockade after bilateral cervical vagotomy. In contrast, the CHF group did not exhibit significant changes in urine flow or free-water clearance during balloon inflation. Plasma antidiuretic hormone (ADH) was significantly elevated in the CHF group; however, balloon distension reduced plasma ADH in both groups of dogs. Plasma renin activity was significantly elevated in the CHF dogs and was not changed by balloon distension in either group of dogs. It is concluded that animals with high-output CHF do not exhibit the atrial-diuretic reflex in spite of their ability to reduce ADH levels by atrial distension.

Topics: Animals; Blood Pressure; Dogs; Edema; Female; Heart Failure; Heart Rate; Kidney; Male; Sodium; Vasopressins; Water

Idiopathic edema is characterized by impaired water excretion, particularly in the upright posture. Indirect evidence has shown that antidiuretic hormone is involved in this disease. For this reason, we measured urinary arginine vasopressin by radioimmunoassay before and during water loading (15 ml/kg) in 10 normal women and in 10 subjects with idiopathic edema in both the supine and upright postures. Daily sodium intake was 100 meq. Renin and aldosterone were concomitantly investigated, and abnormally high values were observed both in the recumbent and upright postures. Basal values for urinary arginine vasopressin were identical in control subjects and in patients with idiopathic edema. The water load significantly reduced urinary arginine vasopressin in normal women in both positions, but in those with idiopathic edema only in the supine position. In those with idiopathic edema, assumption of the upright posture was accompanied by a transient decrease in glomerular filtration, a major decrease in osmolar clearance and no decrease in urinary arginine vasopressin after water loading. Significant correlations were established between urinary arginine vasopressin and osmolar or volemic parameters in normal women, but these correlations were not found in those with idiopathic edema in either position. Arginine vasopressin regulation was abnormal in idiopathic edema, and this hormone was believed to play a part in the pathogenesis of this disease.

Topics: Adult; Aldosterone; Arginine Vasopressin; Blood Proteins; Edema; Female; Hematocrit; Humans; Kidney; Kidney Function Tests; Osmolar Concentration; Posture; Radioimmunoassay; Renin; Sodium; Vasopressins; Water

Topics: Edema; Estrogens; Female; Humans; Male; Prolactin; Sex Factors; Vasopressins

Topics: Ascites; Demeclocycline; Edema; Humans; Hyponatremia; Osmolar Concentration; Vasopressins; Water Intoxication

Plasma and urinary arginine vasopressin (AVP) in normal subjects and in patients with various water metabolism disorders was measured using a sensitive, specific radioimmunoassay. The AVP plasma levels in normal subjects were 3.1 +/- 1.2 pg/ml. The parallel changes in plasma osmolality, plasma AVP concentration, and urinary osmolality were observed after water load. In patients with various kinds of hyponatremia and impaired water excretion, plasma AVP concentrations were within or over normal levels, suggesting that persistent secretion of AVP may play an important role in the pathogenesis of hyponatremia. Variable levels of plasma AVP were observed in patients with essential hypernatremia, which in turn suggested that osmoreceptors may be selectively damaged in some patients, and that ADH-secreting neurons are also involved in others. Our radioimmunoassay facility made it possible for us to measure plasma and urinary DDAVP in the treatment of diabetes insipidus.

Topics: Adrenal Insufficiency; Adult; Animals; Arginine Vasopressin; Ascites; Diabetes Insipidus; Dogs; Edema; Humans; Hypernatremia; Hyponatremia; Hypotension, Orthostatic; Infant; Neoplasms; Osmolar Concentration; Radioimmunoassay; Vasopressins; Water

Topics: Adult; Angiotensin II; Edema; Female; Humans; Kallikreins; Kinins; Male; Middle Aged; Renin; Vasopressins

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

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

The concentration of serum sodium is determined by the external balance of water. Hyponatremia occurs when total body water is in excess of sodium, and hypernatremia develops when body water is relatively decreased in relation to sodium. Both disorders may be present in patients with various disease states in which total body sodium is either decreased, normal or increased. The symptomatology in both disorders is related to the disturbance in central nervous system due to brain edema in patients with hyponatremia and brain dehydration, and cerebrovascular hemorrhages in patients with hypernatremia. The treatment of hypo and hypernatremia is achieved by correcting the abnormalities in body water content.

Topics: Adult; Blood Volume; Edema; Endocrine System Diseases; Humans; Hypernatremia; Hyponatremia; Infant; Kidney Concentrating Ability; Kidney Diseases; Syndrome; Thirst; Vasopressins; Water; Water Loss, Insensible

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

A clinical and investigative study is reported of 19 patients with 'idiopathic oedema of women'. The resons for defining this as a specific syndrome unrelated to the menstrual cycle are given, and the clinical features reviewed. During a forced water diuresis the flow and composition of the urine and the plasma volume were studied on tilting from the supine to the upright position seven premenopausal and four postmenopausal patients with this disorder. No differences were found in the results obtained in the follicular and luteal phases of the menstrual cycle or in the pre- and post-menopausal patients. The reductions in urinary volume and electrolyte excretion on upright tilting were greater than those observed under similar circumstances during the luteal phase of the menstrual cycle in normal female controls, and attributed to increased proximal renal tubular reabsorption. The rate of loss of isotopically labelled albumin from the intravascular compartment was greater in patients with idiopathic oedema than in control subjects. A reduction in blood volume on tilting occurred in control subjects and patients with idiopathic oedema, but was greater in the latter; and the larger the fall, the greater were the reductions in urinary flow and electrolyte excretion. The effect of administering 9-alpha-fluorohydrocortisone was studied in nine patients with idiopathic oedema. One patient failed to 'escape' from the sodium-retaining action of this mineralocorticoid and developed pulmonary oedema; the others 'escaped' normally. The pathophysiological disturbance in this condition is related to increased loss of fluid from the vascular compartment but the precise aetiological mechanism remains unknown.

Topics: Adult; Age Factors; Blood Volume Determination; Body Water; Diuretics; Edema; Female; Fludrocortisone; Follicular Phase; Hematocrit; Humans; Luteal Phase; Male; Middle Aged; Plasma Volume; Posture; Psychology; Serum Albumin; Sodium; Syndrome; Vasopressins; Water-Electrolyte Balance

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

Topics: Edema; Heart Diseases; Humans; Vasopressins; Water-Electrolyte Balance

Topics: Aged; Creatinine; Desoxycorticosterone; Diuresis; Edema; Heart Failure; Humans; Hypertension; Infusions, Parenteral; Male; Middle Aged; Osmolar Concentration; Prostatic Hyperplasia; Prostatic Neoplasms; Prostatitis; Sodium; Time Factors; Urea; Urinary Catheterization; Urination Disorders; Vasopressins; Water-Electrolyte Balance

Topics: Edema; Furosemide; Hemodynamics; Humans; Hyponatremia; Kidney; Osmolar Concentration; Sodium; Vasopressins; Water

Topics: Animals; Blood Circulation; Bradykinin; Burns; Drug Synergism; Duodenum; Edema; Epinephrine; Female; Guinea Pigs; Ileum; In Vitro Techniques; Inflammation; Phenoxybenzamine; Propranolol; Rats; Uterus; Vasopressins

Topics: Adrenal Glands; Aldosterone; Ascites; Blood Pressure; Calcium; Creatinine; Cyclic AMP; Edema; Glomerular Filtration Rate; Humans; Hydrocortisone; Hypertension; Kidney; Kidney Failure, Chronic; Kidney Tubules; Liver Cirrhosis; Magnesium; Osmolar Concentration; Phosphates; Potassium; Prostaglandins; Renin; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Adrenal Insufficiency; Animals; Ascites; Diuresis; Edema; Heart Failure; Humans; Male; Methods; Rats; Vasopressins

Topics: Acromegaly; Edema; Endocrine System Diseases; Humans; Hyperaldosteronism; Hyperthyroidism; Hyponatremia; Hypothyroidism; Syndrome; Vasopressins

Topics: Adult; Brain Diseases; Edema; Female; Humans; Hypothalamus; Male; Middle Aged; Vasopressins

Topics: Edema; Female; Humans; Hyponatremia; Middle Aged; Neurologic Manifestations; Polyradiculopathy; Pulmonary Edema; Vasopressins

Topics: Aldosterone; Animals; Cats; Dogs; Edema; Heart Atria; Heart Failure; Humans; Kidney; Mechanoreceptors; Pulmonary Artery; Renin; Vasopressins

Topics: Animals; Cortisone; Drug Synergism; Edema; Gastric Juice; Gastric Mucins; Gastric Mucosa; Microscopy, Electron; Necrosis; Pepsin A; Peptic Ulcer; Peptic Ulcer Hemorrhage; Rabbits; Vasoconstrictor Agents; Vasopressins

Topics: Anuria; Diuresis; Edema; Female; Humans; Kidney Tubules; Middle Aged; Vasopressins

Topics: Aldosterone; Aminohippuric Acids; Animals; Aorta; Ascites; Blood Pressure; Dogs; Edema; Female; Glomerular Filtration Rate; Heart Failure; Norepinephrine; Renin; Sodium; Tricuspid Valve; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Biological Assay; Diuresis; Edema; Humans; Infant Nutrition Disorders; Kwashiorkor; Male; Plasma Volume; Rats; Vasopressins

Topics: Alkalosis; Bicarbonates; Blood Pressure; Blood Urea Nitrogen; Diet, Sodium-Restricted; Diuresis; Edema; Ethacrynic Acid; Female; Furosemide; Humans; Hyponatremia; Hypotension, Orthostatic; Kidney Concentrating Ability; Middle Aged; Potassium Deficiency; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Age Factors; Aldosterone; Body Weight; Capillary Permeability; Edema; Female; Humans; Hyperaldosteronism; Male; Middle Aged; Mineralocorticoid Receptor Antagonists; Natriuresis; Posture; Renin; Sex Factors; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Adrenal Gland Diseases; Adrenocorticotropic Hormone; Aldosterone; Angiotensin II; Biological Assay; Brain Neoplasms; Bronchial Neoplasms; Central Nervous System Diseases; Child; Edema; Endocrine System Diseases; Glioblastoma; Humans; Male; Osmolar Concentration; Pituitary Diseases; Renin; Sodium Chloride; Vasopressins

Topics: Animals; Diuresis; Dogs; Edema; Humans; Positive-Pressure Respiration; Vasopressins

Topics: Aldosterone; Blood Proteins; Body Fluids; Edema; Heart Function Tests; Humans; Kidney Function Tests; Liver Function Tests; Proteinuria; Vasopressins

Topics: Edema; Humans; Liver Cirrhosis; Male; Polyuria; Vasopressins

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

Topics: Adrenal Cortex Hormones; Alkalosis; Blood Urea Nitrogen; Blood Volume; Diuretics; Edema; Ethacrynic Acid; Furosemide; Glomerular Filtration Rate; Humans; Hyperaldosteronism; Hyperkalemia; Hypokalemia; Hyponatremia; Kidney Failure, Chronic; Kidney Tubules; Liver Cirrhosis; Spironolactone; Triamterene; Vasopressins

Topics: Diuresis; Edema; Humans; Nicotine; Pituitary Gland, Posterior; Smoking; United States; Vasopressins

Topics: Adrenocorticotropic Hormone; Anaphylaxis; Animals; Capillary Permeability; Dextrans; Edema; Female; Growth Hormone; Hypophysectomy; Pituitary Hormones, Anterior; Prolactin; Rats; Stimulation, Chemical; Thyrotropin; Vasopressins

Topics: Adolescent; Adult; Aged; Body Weight; Child; Diuretics; Edema; Female; Heart Failure; Hematocrit; Humans; Lung; Lung Compliance; Male; Middle Aged; Oxygen; Positive-Pressure Respiration; Pulmonary Edema; Radiography; Respiration, Artificial; Respiratory Function Tests; Respiratory Insufficiency; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Body Fluids; Capillary Permeability; Dogs; Edema; Glomerular Filtration Rate; Humans; Lymphatic System; Pressure; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Biological Assay; Eclampsia; Edema; Female; Heart Failure; Humans; Male; Methods; Nephrotic Syndrome; Pregnancy; Rats; Vasopressins

Topics: Adult; Aldosterone; Body Weight; Diuretics; Edema; Female; Heart Function Tests; Histamine; Humans; Kinins; Liver Function Tests; Prediabetic State; Pregnancy; Psychophysiologic Disorders; Vasopressins; Water-Electrolyte Balance

Topics: Dextrans; Edema; Fallopian Tubes; Felypressin; Female; Humans; Isotonic Solutions; Peritoneal Neoplasms; Postoperative Complications; Pregnancy; Pregnancy, Tubal; Sterilization, Reproductive; Therapeutic Irrigation; Tissue Adhesions; Vasopressins

Topics: Adolescent; Adult; Aged; Edema; Female; Heart Failure; Humans; Male; Middle Aged; Nephrotic Syndrome; Pregnancy; Vasopressins

Topics: Animals; Creatinine; Diet, Sodium-Restricted; Diuresis; Dogs; Edema; Glomerular Filtration Rate; In Vitro Techniques; Kidney; Kidney Concentrating Ability; Natriuresis; Organ Size; Perfusion; Potassium; Pressure; Promethazine; Regional Blood Flow; Urea; Vasopressins

Topics: Adolescent; Adult; Drug Hypersensitivity; Edema; Estrogens; Female; Follicle Stimulating Hormone; Growth Hormone; Hormones; Humans; Middle Aged; Progesterone; Progestins; Urticaria; Vasopressins

Topics: Amphetamine; Amyl Nitrite; Atropine; Edema; Female; Humans; Liver Diseases; Myxedema; Pre-Eclampsia; Pregnancy; Premenstrual Syndrome; Sodium Chloride; Vasopressins

Topics: Addison Disease; Adolescent; Adrenalectomy; Adult; Aldosterone; Creatine; Dextroamphetamine; Diabetes Insipidus; Edema; Ethanol; Female; Humans; Kidney Tubules; Middle Aged; Natriuresis; Posture; Spironolactone; Vasopressins

Topics: Adolescent; Adult; Animals; Aortic Diseases; Ascites; Biological Assay; Blood; Dogs; Edema; Female; Heart Failure; Hematocrit; Humans; Male; Mitral Valve Insufficiency; Potassium; Secretory Rate; Sodium; Urine; Vasopressins; Venae Cavae

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

Topics: Diuretics; Edema; Heart Failure; Kidney Diseases; Liver Diseases; Organomercury Compounds; Physiology; Vasopressins

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

Topics: Blood Chemical Analysis; Digestive System Surgical Procedures; Disease Susceptibility; Edema; Gastrectomy; Humans; Liver; Postoperative Complications; Stomach; Vasopressins

Topics: Blood Pressure; Body Weight; Diuresis; Edema; Female; Glomerulonephritis; Humans; Hypertension; Hypertension, Renal; Inulin; Kidney; Kidney Function Tests; Nephrosclerosis; Osmolar Concentration; Pathology; Pharmacology; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Cardiovascular; Proteinuria; Vasopressins

Topics: Arginine Vasopressin; Blood Chemical Analysis; Edema; Heart Failure; Humans; Obesity; Vasopressins

Topics: Adrenocorticotropic Hormone; Dextrans; Edema; Exudates and Transudates; Formaldehyde; Pituitary Gland; Pituitary Gland, Posterior; Rats; Vasopressins

Topics: Arginine Vasopressin; Edema; Heart Failure; Humans; Liver Cirrhosis; Vasopressins

Topics: Animals; Arginine Vasopressin; Chlorothiazide; Desoxycorticosterone; Desoxycorticosterone Acetate; Dexamethasone; Edema; Hydrocortisone; Prednisolone; Rats; Vasopressins

Topics: Arginine Vasopressin; Edema; Humans; Vasopressins

Topics: Edema; Humans; Vasopressins

Topics: Aldosterone; Arginine Vasopressin; Edema; Humans; Vasopressins

Topics: Arginine Vasopressin; Edema; Humans; Vasopressins

Topics: Animals; Arginine Vasopressin; Edema; Female; Humans; Menstruation; Ovulation; Papio; Papio hamadryas; Papio ursinus; Polyuria; Urination Disorders; Vasopressins

Topics: Arginine Vasopressin; Edema; Liver Diseases; Vasopressins

Topics: Animals; Arginine Vasopressin; Dogs; Edema; Liver; Vasopressins

Topics: Edema; Heart Failure; Hormones; Liver Cirrhosis; Pituitary Gland; Pituitary Gland, Posterior; Vasopressins; Water

Topics: Body Fluids; Edema; Hormones; Humans; Pituitary Gland; Vasopressins

Topics: Edema; Humans; Vasopressins

Topics: Edema; Electrolytes; Liver Diseases; Renal Elimination; Vasopressins; Water