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)

When extracerebral dopa decarboxylase is inhibited by carbidopa, L-dopa lowers plasma renin activity (PRA). The present study was designed to determine whether this suppression of PRA is mediated by the sympathetic nerves, and to identify the peripheral adrenergic receptor types involved. All experiments were performed in pentobarbital-anesthetized dogs in which changes in renal perfusion pressure were minimized by means of a suprarenal aortic clamp. Neither alpha adrenoreceptor blockage with phenoxybenzamine nor beta adrenoreceptor blockade with propranolol was by itself sufficient to block the suppression of PRA by L-dopa with carbidopa. However, combined alpha and beta adrenoreceptor blockade lowered PRA and completely prevented any further suppression of PRA by L-dopa with carbidopa. It was also observed that phenoxybenzamine decreased PRA by 48% when administered to propranolol-treated animals. Taken together, these data indicate that L-dopa with carbidopa suppresses PRA by decreasing sympathetic nerve stimulation of both alpha and beta adrenoreceptors. Plasma vasopressin concnetration was significantly decreased by L-dopa with carbidopa both in the control group and in animals with combined alpha and beta adrenoreceptor blockade. Because plasma vasopressin levels decreased after L-dopa, vasopressin is unlikely to play a causative role in the suppression of PRA.
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PMID:Role of peripheral adrenoreceptors and vasopressin in the suppression of plasma renin activity by L-dopa in carbidopa-treated dogs. 48 Jan 87

Plasma renin activity was determined in 25 healthy, full-term, newborn infants aged 1 day to 9 weeks. High values were found, the mean level at 1-2 days of life (24.8 +/- 8.4 ng/ml/hr, SE) being significantly higher than the mean levels at 7-9 days (5.8 +/- 1.5) and at 4-9 weeks (8.1 +/- 1.3) (P less than 0.05). No correlation was found between plasma renin activity and systolic blood pressure, hematocrit, creatinine clearance, serum sodium, or serum potassium. Plasma renin activity (log values) was inversely correlated with sodium intake (r = -0.58) or with urinary sodium (r = -0.44), and positively with urinary osmolality (r = 0.67). The correlations reached higher coefficients if only infants aged less than or equal to 9 days were considered. In addition, vasopressin was measured by radioimmunoassay in the urine. The daily excretion was lower in newborn infants (9.4 +/- 1.6 ng/m2/day, SE, at 1-2 days of postnatal life) than in healthy children (37.1 +/- 5.6), and was significantly correlated with creatinine clearance (r = 0.69), but not with urinary osmolality.
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PMID:Plasma renin activity related to sodium balance, renal function and urinary vasopressin in the newborn infant. 48 42

Eighteen healthy male subjects, were investigated under normal sodium intake and after 5 days of high and low sodium intake. Under normal sodium intake, the following mean values were observed -- plasma osmolality (Posm): 294 +/- 5 mOsm/kg -- plasma volume (Vp): 33.9 +/- 4,3 ml/kg -- urinary sodium output (UNa.V): 173 +/- 73 mEq/24 h -- urinary antidiuretic hormone (A.D.H.): 68.8 +/- 35.6 ng/24 h. Under low sodium intake these values decreased to -- Posm: 289 +/- 4 m Osm/kg -- Vp: 32.7 +/- 3.2 ml/kg -- UNa.V: 12 +/- 9 mEq/24 h -- A.D.H.: 40.9 +/- 16.3 ng/24 h. Under high sodium intake these values increased to -- Posm: 298 +/- 5 m Osm/kg -- Vp: 36.3 +/- 4.1 ml/kg -- UNa.V: 325 +/- 67 mEq/24 h -- A.D.H.: 118.2 +/- 45.5 NG/24 H. Highly significant correlations are found between Posm and A.D.H. and between the Posm or A.D.H. and UNa.V. Interest is focused on UNa.V since the correlation between A.D.H. and UNa.V (r = 0.78) is more significant than that between A.D.H. and Posm (r = 0.47). Overriding of Posm on Vp in the regulation of A.D.H. secretion is again demonstrated. Plasma renin activity decrease when A.D.H. increase.
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PMID:[Variations in urinary antidiuretic hormone levels related to sodium intake (author's transl)]. 49 37

1. The effect of restricted water intake followed by voluntary rehydration with water or 10 mM-KCl was studied in four conscious sheep with respect to plasma concentrations of renin, antidiuretic hormone (ADH), protein and electrolytes, and urine flow rate, osmolality and osmolal excretion. 2. Water restriction increased the plasma renin concentration and the plasma ADH concentration. 3. Rehydration with water caused a further rise in plasma renin, but plasma ADH returned to basal levels in less than 2 hr. 4. Rehydration with 10 mM-KCl in order to stabilize plasma K concentration greatly attenuated the post-drinking rise in plasma renin concentration, while plasma ADH levels fell as before. 5. Urine flow rates after rehydration with water and 10 mM-KCl remained low for at least 6 hr in most experiments despite low plasma ADH levels. The effect on urine osmolality ranged from no change to a large drop. 6. The post-drinking antidiuresis was associated with a reduction in solute excretion rate. However, free water clearance usually remained negative. 7. These experiments do not support the existence of a direct nexus between plasma ADH levels and plasma renin concentration.
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PMID:Renin, antidiuretic hormone and the kidney in water restriction and rehydration. 51 41

The kidney has a high capacity to produce a spectrum of different acting prostaglandins (PG). In vivo and in vitro studies have shown that renal formation of PG's, possibly in the vasculature of the cortex represents an essential step in the mechanisms regulating the secretion of renin. PG's formed in the cortex seem to participate also in the control of renal vascular resistance and glomerular filtration rate. PGE2 formed in the medulla modulates the hydroosmotic action of antidiuretic hormone and influences the kidney's capacity for urine concentration. Renal PG formation is reduced by high NaCl intake and enhanced by low NaCl intake and in hypokalemic states. These findings make renal PG's good candidates for participation in the regulation of salt and water balance and in the control of blood pressure. Due to the close connection with the renin angiotensin system, alterations in renal PG formation might be involved in the etiology of high and low renin states. Thus, an impairment in the renal cortical production of vasodilating and renin-stimulating PG's could constitute the common denominator for both the reduced renin secretion and the increased vascular resistance which have been reported to be associated in essential hypertension.
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PMID:Formation and action of prostaglandins in the kidney. 53 77

The direct action of arginine-vasopressin (AVP) and its deamino-D-arginine analogue (DDAVP) on renin release (RR) has been studied in isolated rat kidneys perfused with an electrolyte solution at constant pressure in a single-pass system. AVP and DDAVP infused at various concentrations (80 to 2100 pg/ml and 80 to 8700 pg/ml, respectively) reduced volume and increased osmolality of urine in a dose-dependent way. High doses of AVP reduced renal perfusate flow and glomerular filtration rate while DDAVP had no effect on renal haemodynamics. When vasoconstrictor doses of AVP or high concentrations of DDAVP were infused, "basal" RR remained unchanged. However, when RR had been stimulated by infusion of isoproterenol, vasoconstrictor doses of AVP as well as high doses of DDAVP which did not increase renal vascular resistance diminished RR by about 30% (P less than 0.01, and P less than 0.05, respectively). These results suggest that the inhibition of RR by vasopressin is not related to its vasoconstrictor action.
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PMID:Effects of vasopressin and its deamino-D-arginine analogue on renin release in the isolated perfused rat kidney. 56 83

Male Sprague-Dawley rats with unilateral renal artery stenosis and a contralateral untouched kidney develop a malignant hypertension (MH) which is characterized by high blood pressures, sodium and water depletion, and subsequent activation of the renin-angiotensin system. In the present studies we found plasma arginine vasopressin (AVP) concentrations-3-fold higher than those in rats with benign renal hypertension, and 4- to 5-fold higher than those in normotensive control rats. Analysis of individual values showed considerable scatter; about 50% of the values fell in the range of benign hypertensive or control rats. When a specific AVP antiserum was injected, iv, into eight conscious unrestrained MH rats, BP transiently fell toward control values in four; in one, BP fell by only 10 mm Hg, and three other MH rats showed no response. In the same rats, injection of a specific angiotensin II antiserum always induced a transient fall in BP. On the basis of these and previously reported observations, we conclude that, subsequent to sodium and water loss and activation of the renin-angiotensin system, vasopressin release is stimulated in a significant number of MH rats and that, in these rats, vasopressin may cause significant systemic vasoconstriction. Thereby vasopressin may contribute to the development of malignant renal hypertension in rats.
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PMID:Plasma vasopressin concentrations and effects of vasopressin antiserum on blood pressure in rats with malignant two-kidney Goldblatt hypertension. 61 98

Normal Long-Evans rats (LE) exhibited diurnal variations of plasma arginine vasopressin (AVP) concentrations with peak values at 10 A.M. and minimum values at 1 P.M. Brattleboro rats heterozygous for hypothalamic diabetes insipidus (DI) had significantly reduced plasma AVP concentrations and increased plasma osmolalities when compared with LE rats. By prolonged injection of 100 mU/day of vasopressin tannate (VPT) into Brattleboro rats homozygous for DI, plasma AVP concentrations close to those of LE rats were achieved. Potassium was retained for 7 days until escape of vasopressin-induced potassium retention occurred. When 500 mU VPT were injected into DI rats, high plasma AVP levels were induced. Potassium was retained for 2-3 days. After initial sodium retention, periods of natriuresis occurred. During treatment with 100 mU VPT/day most of the alterations present in DI rats were corrected, which included increased water turnover and external water loss, increased hematocrit and plasma sodium concentrations (but not increased plasma osmolalities), hypokalemia, increased activity of the renin-angiotensin system, and reduced adrenocortical function.
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PMID:Effects of prolonged vasopressin treatment in Brattleboro rats with diabetes insipidus. 62 99

In non-hydrated goats prolonged (3 h, 0.02 ml/min) intracerebroventricular (IVT) infusion of 0.35 M glycerol depressed the plasma vasopressin level during the entire infusion period which resulted in a conspicuous water diuresis outlasting the infusion by about 20 min. Since no compensatory drinking occurred during this sustained water diuresis it gradually induced pronounced dehydration (loss of greater than 1 liter of total body water causing 5% increase in plasma [Na+] and osmolality). The same degree of dehydration was in other experiments induced by water deprivation. It then caused a 5-fold increase in plasma vasopressin level. Corresponding IVT infusions of 0.35 M d-glucose depressed plasma vasopressin level only during the first half of the 3 h infusion period. Consequently, the resulting water diuresis was transient and subsided before the glucose infusion was finished. Plasma renin activity increased during the IVT glycerol infusion and during water deprivation, but was largely unaffected by IVT glucose. Both IVT glycerol and glucose decreased renal sodium excretion. The possibility is discussed that the pronounced ability of IVT glycerol to depress the vasopressin release and thirst is not only due to dilution induced reduction of CSF [Na+], but also to an influence of glycerol on choroidal and/or transependymal Na+-transporting mechanisms.
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PMID:Inhibition of vasopressin-release during developing hypernatremia and plasma hyperosmolality: an effect of intracerebroventricular glycerol. 65 32

Eight men, 19-35 years of age, breathed 20.9% (normal oxygen), 13.9% (mild hypoxia) or 11.1% (severe hypoxia) oxygen in nitrogen gas mixtures during three 20 min periods, which were separated by 1 h recovery periods. The order in which the gas mixtures were breathed was random. The partial pressure of oxygen decreased from a mean of 93.5 during exposure to normal oxygen to 53.9 and 36.7 mmHg during mild and severe hypoxia respectively. There were corresponding decreases in haemoglobin saturation. The partial pressure of carbon dioxide was lower and the pH higher during severe hypoxia than during exposure to normal oxygen. There were no changes in the plasma osmolality or in the concentrations of sodium or potassium in the plasma. There was a tendency for both the renin activity and the concentration of aldosterone in the plasma to decrease progressively as the percentage of oxygen breathed decreased. Unlike severe hypoxia, mild hypoxia suppressed the concentration of antidiuretic hormone (ADH) in the plasma of all subjects by about 59%; during severe hypoxia the reduction was not significant, being only about 33%. These data are consistent with the suggestion that the effect of hypoxia on the release of ADH is dependent on the level of hypoxia.
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PMID:Response of antidiuretic hormone to acute exposure to mild and severe hypoxia in man. 66 35


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