Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three children aged 2 1/2 to 5 1/2 yr, with burns covering 30%--45% of body surface area, developed hyponatremia and serum hypotonicity on the 5th--6th day following the burn injury. The hyponatremia persisted for 10--15 days. During this period, all three passed inappropriately concentrated urines. One child also demonstrated marked and inappropriate thirst. All three children demonstrated persistent respiratory alkalosis, which appeared and disappeared concomitantly with the hyponatremia. There were no signs of dehydration, and plasma volumes, measured in two children, were normal to high. These children are believed to show evidence of inappropriate antidiuretic hormone (ADH) secretion. In the absence of those conditions known to produce this syndrome, it is postulated that in these children it may have resulted from prolonged pain, anxiety, and/or pyrexia.
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PMID:Persistent hyponatremia and inappropriate antidiuretic hormone secretion in children with extensive burns. 45 38

A 12-year-old female with lymphosarcoma responding to treatment including vincristine and cyclophosphamide developed clinical and laboratory findings compatible with the syndrome of inappropriate secretion of antidiuretic hormone. Some additional findings were observed, i.e. uremia, hypopotassemia and alkalosis, that have not so far been recorded in that syndrome. All abnormalities were corrected upon water restriction. A similar episode occurred after a 2nd drug course. It too was corrected upon water restriction. The patient was clinically free from her malignancy in both episodes. It is suggested that our child had probably an expanded form of the syndrome of inappropriate secretion of antidiuretic hormone.
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PMID:Electrolyte abnormalities in lymphosarcoma after chemotherapy. 58 54

It has been shown that endothelin-1 (ET-1) binding sites exist in the central nervous system and that the injection of intracerebroventricular ET-1 induces a pressor response. Therefore, we determined the neurohormonal and cardiovascular responses to intracerebroventricular ET-1 (25 pmol/kg) in conscious rabbits with chronically instrumented electrodes on the renal sympathetic nerve. Intracerebroventricular ET-1 provoked a prompt increase in arterial pressure and in renal sympathetic nerve activity within 5 minutes, and peak values were obtained at 20 and 40 minutes, respectively. Plasma epinephrine and norepinephrine reached peak values at 5-20 minutes. Plasma vasopressin and plasma glucose levels also increased significantly, but plasma osmolality, hematocrit, and serum sodium and potassium concentrations did not show any changes. Arterial blood gas analysis showed respiratory alkalosis. However, pretreatment with intravenous pentolinium (5 mg/kg), a ganglion blocking agent, abolished these neurohormonal and cardiovascular responses. Conversely, the same dose of intravenous ET-1 (25 pmol/kg) as that used in the intracerebroventricular experiment failed to cause any cardiovascular or renal sympathetic nerve responses. These results suggest that intracerebroventricular ET-1 acts in the central nervous system and causes a pressor response mainly through the enhancement of sympathoadrenal outflow.
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PMID:Central effect of endothelin on neurohormonal responses in conscious rabbits. 204 64

Chronic chloride depletion alkalosis in dogs causes a lowered osmotic threshold and increased sensitivity for vasopressin (AVP) release. Since AVP release and drinking behavior normally are closely associated over a narrow range of changes in plasma osmolality (Posm), we investigated whether alkalotic dogs would also show an altered responsiveness to the dipsogenic effects of angiotensin II (ANG II) and osmotic stimuli. Dogs made chronically alkalotic by a combination of chloride-free diet and furosemide injections developed polydipsia in the absence of any increase in solute intake and in the presence of a significant reduction in Posm. The animals were chronically hypochloremic, hyponatremic and hypokalemic, and appeared to be extracellular fluid (ECF) contracted. Plasma renin activity (PRA) was 10-fold higher in alkalotic dogs than controls. When Posm was increased by a slow 2 hr infusion of hypertonic sodium sulfate, alkalotic dogs were found to have a significantly lower osmotic threshold for inducing drinking (289.8 +/- 1.1 mOsm/kg/H2O vs. 305.1 +/- 1.3 mOsm/kg/H2O in controls), but the slope or sensitivity of the water intake/Posm relationship was not significantly different. Finally, compared to normal animals, alkalotic dogs were unresponsive to the dipsogenic effects of IV ANG II. These data indicate that the central mechanisms which mediate drinking in response to cellular and extracellular thirst stimuli are altered in chronic metabolic alkalosis.
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PMID:Altered drinking responses in dogs with chronic metabolic alkalosis. 285 45

Hyperhydrated goats were exposed to an environmental temperature of 45 degrees C (relative humidity 70%) for 120 min. After 90 min, rectal temperature and respiratory frequency reached plateau levels of 40.5 degrees C and 280 respirations min-1, respectively. Measurements of arterial and venous blood acid-base parameters revealed that respiratory alkalosis had started to develop after 60 min, and had become obvious at the end of the heat exposure period. Renal compensation (evidenced by gradual increases in urinary pH and renal Na excretion) developed in parallel with the respiratory alkalosis. The heat exposure elicited a moderate, temporary inhibition of the water diuresis, but no obvious increase in the renal excretion of arginine vasopressin (antidiuretic hormone, ADH). Preliminary determinations of plasma aldosterone did not show any change during the actual heat exposure period, but a 50% temporary decrease in plasma aldosterone 30 min thereafter. The study confirms the susceptibility of goats to develop respiratory alkalosis during thermoregulatory panting, and shows that this is not to any appreciable extent diminished during hyperhydration. It can further be concluded that a heat-induced rise in body temperature to 40.5 degrees C is no powerful stimulus for vasopressin release in the hyperhydrated goat. The determinations of plasma aldosterone suggest that reduced liberation of the hormone does not contribute to the immediate renal compensation of respiratory alkalosis, but that respiratory alkalosis reaching a certain intensity inhibits aldosterone secretion.
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PMID:Influence of heat exposure on acid/base and fluid balance in hyperhydrated goats. 371 31

A decrease in extracellular pH is well known to inhibit vasopressin stimulated water flow in the toad bladder. It remains unclear whether this inhibition is the result of the effect of extracellular pH per se or the consequence of altered intracellular pH. In the present study we evaluated the effect of several maneuvers capable of altering intracellular pH on vasopressin or cyclic AMP stimulated water flow in the toad bladder in the absence of alterations of extracellular pH. In the presence of a normal extracellular pH, bladders subjected to a high partial pressure of CO2 or bladders from acidotic toads had a significant decrease in vasopressin or cyclic AMP stimulated water flow as compared to controls. We also examined the effect of maneuvers capable of increasing intracellular pH on vasopressin and cyclic AMP stimulated water flow. Intracellular alkalosis was induced by exposing the bladders in vitro to NH4Cl at pH 8 or to acetazolamide. Both maneuvers resulted in a significant decrease in vasopressin, but not in cyclic AMP stimulated water flow. Bladders removed from alkalotic toads, incubated in a normal extracellular pH also showed a decrease in AVP stimulated water flow. Intracellular muscle pH assessed with phosphorus nuclear magnetic resonance, was not different among bladders from control, acidotic and alkalotic toads. It is concluded that alterations of intracellular pH, in the absence of alterations of extracellular pH, are important in regulation of water transport in the toad bladder in response to vasopressin or cyclic AMP. In addition, metabolic acidosis or alkalosis alters AVP or cyclic AMP stimulated water flow by a mechanism independent of the intracellular pH.
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PMID:Acid-base metabolism, intracellular pH and water transport by the toad bladder. 631 61

Early alterations in fluid, electrolytes, and their regulating hormones were investigated in men exposed to 6,000 m simulated altitude (2 h-ascent, 2 h-sojourn, 2 h-return). Hematocrit and serum protein rose with elevated serum osmolality and reduced urine flow upon arrival at 6,000 m, suggesting decreased plasma volume probably due to hypotonic fluid shift to intracellular spaces. Serum K declined reflecting respiratory alkalosis. The exposure raised plasma antidiuretic hormone (ADH), plasma renin activity (PRA), serum cortisol and aldosterone. Increases both in ADH and aldosterone showed close correlations with that in cortisol, suggesting that ADH may be elevated by hypoxic stress in addition to elevated serum osmolality and decreased plasma volume, and that increased secretion of adrenocorticotropin may be the main cause of increased aldosterone, though PRA involvement cannot be excluded. These rises in ADH and aldosterone may act to retain body water, and the latter may exaggerate alkalosis; thus, these hormonal changes may be related to acute mountain sickness.
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PMID:Hormonal disturbances of fluid-electrolyte metabolism under altitude exposure in man. 637 81

Urinary excretion rate of antidiuretic hormone (UADHV) was studied in male volunteers in response to hypobaric hypoxia. The first series consisted of three groups. The chamber was decompressed to 465, 495, and 438 Torr during high-altitude (HA) exposure for groups I (n = 5), II (n = 5), and III (n = 4), respectively. In group I, the chamber air contained 3.77% CO2 to prevent alkalosis. The level of hypoxemia was similar in groups I and II. Mean 24-h UADHV was unchanged in group I, but increased 96% (P less than 0.05) and 180% (P less than 0.05) in groups II and III, respectively, on day 1 at HA and was normal during subsequent days at HA regardless of symptoms of acute mountain sickness. Shorter sampling intervals employed in a second series of experiments conducted at 495 Torr revealed a twofold increase in UADHV (P less than 0.05) 8-12 h after ascent in eight asymptomatic subjects; UADHV returned to base line within 9 h and remained low. The symptomatic subjects both had increased UADHV (3- and 8-fold from base line) between 2 and 4 h after ascent. Increased UADHV in asymptomatic subjects may be a result of the concomitant decrease in plasma volume, both of which appeared to be eliminated by CO2 supplementation.
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PMID:Antidiuretic hormone responses to eucapnic and hypocapnic hypoxia in humans. 681 99

Acute hypoxia causes increased sodium and water excretion. Animal studies suggest that this renal response is largely driven by direct peripheral arterial chemoreceptor stimulation, independent of accompanying changes in ventilation and acid-base status. Whether the diuresis and natriuresis observed in humans made acutely hypoxic are caused by peripheral chemoreceptor stimulation is not known, but, if so, we hypothesized that people with a high ventilatory response to hypoxia (high peripheral chemosensitivity) should have greater diuresis and natriuresis than those with a low ventilatory response to hypoxia. The isocapnic hypoxic ventilatory response (HVR) of 16 subjects on a fixed sodium intake was measured, as were their urinary volume and sodium and bicarbonate losses during 6 h of breathing air (in a normobaric environmental chamber) and, on the subsequent day, 12% O2. The isocapnic HVR correlated positively with hypoxic diuresis (r = 0.87) and natriuresis (r = 0.76). In contrast, the isocapnic HVR did not correlate with bicarbonate excretion, despite the expected respiratory alkalosis of acute hypoxia. The magnitude of diuresis and natriuresis with hypoxia did not correlate with changes in circulating aldosterone, renin, atrial natriuretic peptide, vasopressin, or a digoxin-like immunoreactive substance. These findings are compatible with a role of the peripheral arterial chemoreceptors in mediating the renal response to hypoxia in humans. The efferent pathway remains unknown.
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PMID:Diuretic effect of acute hypoxia in humans: relationship to hypoxic ventilatory responsiveness and renal hormones. 775 4

1. In the syndrome of inappropriate secretion of antidiuretic hormone, hyponatraemia is associated with a normal bicarbonate concentration despite dilution. This normal bicarbonate concentration is related to the development of a hyperaldosteronism, which is attributed to a direct stimulation of the zona glomerulosa by the hyponatraemic state. Some workers have suggested that, to develop this hyperaldosteronism requires the presence of a pituitary factor. To determine whether the pituitary gland plays a role in this hyponatraemia-induced hyperaldosteronism, water intoxication was performed for 24 h in normal and in panhypopituitaric rats. 2. In normal rats, hyponatraemia (108 mmol/l), induced by the administration of 1-desamino-8-D-arginine vasopressin and 2.5% D-glucose-0.45% NaCl by gavage (15% body weight) was associated with a mild increase in bicarbonate concentration, and blood acid-base equilibrium showed a mixed metabolic and respiratory alkalosis (pH 7.57, partial pressure of CO2 29 mmHg, base excess +5.5 mmol/l), and aldosterone concentration was increased 3-fold as compared with the control value. When hyponatraemia (110 mmol/l) was induced in a similar manner in panhypopituitaric rats, we observed a very low aldosterone concentration (< 50 pg/ml) and a compensated respiratory alkalosis (pH 7.45, partial pressure of CO2 30 mmHg, base excess -2.6 mmol/l). The restoration of a hyperaldosteronaemic state in this group of rats was related essentially to corticosteroid intake. 3. These data suggest that corticosteroids play a critical role in the development of hyponatraemia-related hyperaldosteronism, a phenomenon not necessarily dependent on a pituitary factor.
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PMID:Restoration by corticosteroids of the hyperaldosteronism in hyponatraemic rats with panhypopituitarism. 783 96


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