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)

Intravenous infusions of [Sar1-Ala8]angiotensin II, acute hypophysectomy, and acute intestinal denervation were carried out in 15 pentobarbital-anesthetized cats. Infusion of the angiotensin II antagonist caused only a small increase in superior mesenteric arterial conductance and a small decrease in arterial pressure in intact animals, but the changes were subypophysectomy alone caused only a small intestinal vasodilatation and little change in arterial pressure. However, the responses to hypophysectomy were much larger when the gland was removed during a prolonged infusion of the angiotensin II antagonist. Intestinal denervation caused only minor changes in mesenteric conductance and arterial pressure, and the responses to [Sar1-Ala8]angiotensin II and hypophysectomy were largely unaltered by the presence or absence of the intestinal innervation. The results suggest that the renin-angiotensin and vasopressin systems are reciprocal overlapping mechanisms that exert a significant vasoconstrictor influence on the intestinal resistance vessels in the anesthetized cat. In the absence of one control system, the other appears to compensate to maintain resistance.
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PMID:Vasopressin and angiotensin: reciprocal mechanisms controlling mesenteric conductance. 84 81

1. A lithium chloride (1.1 g/kg) supplemented diet was given to Long Evans (LE) and Brattleboro (DI) rats to investigate its actions in the presence (LE) and absence (DI) of vasopressin. 2. During the first 24 h, Li-supplemented LE rats displayed an initial water deficit (drinking less than renal output), increased plasma antidiuretic (ADH) titres and slightly increased plasma renin activities (PRA) and plasma osmolarities. Such changes were qualitatively similar to those seen in rats fed a normal diet, but deprived of water for 24 hours. After 12 days, the Li-supplemented rats had elevated plasma ADH titres, but reduced pituitary oxytocic and antidiuretic activities. 3. The urinary losses of Na, K and Cl exceeded dietary intakes in LE rats on the introduction of the Li-supplement, and the urinary osmolarity fell by 50%. Electrolyte balances were gradually re-established, although drinking and urine production increased in parallel to reach twice the control values by day 12 of the supplement. 4. Aldosterone and corticosterone secretory rates and their peripheral plasma concentrations were unchanged both after 24 h and 28 days of the Li-supplement. 5. Li elicited no water deficit or saluresis in DI rats, and although the polyuria and polydipsia were exacerbated, urinary osmolarity did not change over the 12 day observation period. 6. Li increased Ca excretion in both rat types; after 12 days the PRA of DI but not LE animals were increased. 7. It is concluded that the overall renal actions of Li are tempered by vasopressin rather than adrenocorticosteroids.
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PMID:Time course of lithium-induced alterations in renal and endocrine function in normal and Brattleboro rats with hypothalamic diabetes insipidus. 85 9

1. Ten patients on maintenance diuretic treatment received an intravenous infusion of antidiuretic hormone at a low rate for 1 hr. 2. A gradual reduction in mean plasma renin activity was observed and this was significant at 60 min. 3. There was a significant correlation between the initial value and the extent of the fall in plasma renin activity. There was no consistent change in blood pressure, heart rate and blood volume. 4. The results point to an intrarenal site of action of antidiuretic hormone.
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PMID:Suppression of plasma renin activity by intravenous infusion of antidiuretic hormone in man. 86 31

Comprehensive studies on body fluid balance on 5 divers were conducted during the Hana Kai II dive (17 days at 18.6 ATA and 7 days of decompression). Daily urine flow increased from about 2000 ml at 1 ATA to 2600 ml at 18.6 ATA, at 31 degrees C. This diuresis was accompanied by a reduction in urine osmolality (from 650 to 500 mOsm) and a slight increase in osmolal clearance. Endogenous creatinine clearance remained at about 173 ml/min throughout the dive. Despite such a sustained diuresis, neither daily water intake nor total body water volume changed significantly. The plasma renin activity changed little, while both plasma aldosterone concentration and urinary aldosterone excretion increased significantly during the first week at 18.6 ATA. The plasma prolactin concentration showed a significant decrease during the first 3 days at 18.6 ATA. The daily excretion of antidiuretic hormone (ADH) decreased significantly (by 40%) 4 days after compression and remained low throughout the rest of the dive. Insensible waterloss at 18.6 ATA was 35% lower than that at 1 ATA. It is suggested that the observed hyperbaric diuresis is due primarily to suppression of ADH as a result of suppression of insensible water loss.
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PMID:Hana kai ii: a 17-day dry saturation dive at 18.6 ATA. III. Body fluid balance. 91 Mar 16

The threshold of serum osmolality causing release of vasopressin (antidiuretic hormone) was shifted to an abnormally low level (262 mosmol/kg H2O) in a 14-year-old girl with hypertension and signs of hypoplastic corpus callosum. There was a physiologically meaningful control of vasopressin release in response to water restriction and water load. Plasma vasopressin concentrations (range 1.2--11.9 pg/ml) were of the same magnitude as those of healthy adults, being abnormally high only when related to the hypotonicity of serum observed. Plasma concentrations of angiotensin II were higher than expected from the suppressed levels of plasma renin activity. Blood-pressure response to angiotensin II infusion was increased. Resetting of the osmostat and hypertension may both be explained by lesions of the central nervous system.
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PMID:Inappropriate secretion of antiduretic hormone, hypertension, and hypoplastic corpus callosum. 91 74

The concentration of both plasma renin and plasma arginine vasopressin rose in normal subjects after an 85 degrees head-up tilt. Plasma renin activity, which increased 70-80% above the supine value, was maximal at 15 or 30 min, whereas the six- to seven-fold increase of plasma arginine vasopressin concentration was observed between 30 and 45 min. Intravenous propranolol administered just before tilt was used to investigate the possibility that the delayed rise of arginine vasopressin was stimulated by renin. Although the response of plasma renin was completely abolished by propranolol, the response of vasopressin was unaffected. These findings suggest that the release of vasopressin that follows isosmolar hypovolemia achieved by orthostasis may occur independently of changes in the renin-angiotensin system in the presence of propranolol.
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PMID:The interrelationship between the release of renin and vasopressin as defined by orthostasis and propranolol. 91 8

Negative sodium balance was produced in 10 human volunteers. Body weight, plasma sodium, osmolality, hematocrit, renin activity (PRA), and antidiuretic hormone (ADH) concentrations were determined before, during, and after sodium restriction. Body weight declined and PRA rose during the period of low sodium intake. Plasma sodium concentration and osmolality did not change. A statistically significant change in ADH was not observed. It is suggested that a decrease in ADH was prevented by a rising titer of renin and contraction of the extracellular space.
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PMID:Concentrations of antidiuretic hormone in plasma during human sodium restriction. 91 79

To study the effect of prolonged recumbency on plasma vasopressin and renin activity, eight women (23-34 yr) were subjected to 17 days of absolute bed rest. The +3 Gz tolerance of the subjects was tested before and after 14 days of bed rest. From day 2 and through day 17 of bed rest, plasma arginine vasopressin (AVP) levels were reduced 33%. Plasma renin activity (PRA) increased 91% (P less than 0.05) above ambulatory control values from days 10 through 15 of bed rest. When compared to precentrifuge values, exposure to +3 Gz prior to bed rest provoked a 20-fold rise (P less than 0.05) in mean plasma AVP but resulted in only a slight increase in PRA. After bed rest, acceleration increased plasma AVP 7-fold (P less than 0.02); however, the magnitude of this increase was less than the post +3Gz value obtained prior to bed rest. After bed rest, no significant rise was noted in PRA following +3 Gz. This study demonstrates that prolonged bed rest leads to a significant rise in the PRA of female subjects, while exposure to +Gz acceleration provokes a marked rise in plasma AVP.
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PMID:Plasma vasopressin and renin activity in women exposed to bed rest and +Gz acceleration. 93 30

In babies ranging in age from 1 to 25 weeks and in children between 1 and 14 years, plasma renin activity and urinary aldosterone activity were determined in relation to urinary sodium excretion. A reciprocal correlation was found demonstrating that the hyperactivity of the renin-angiotensin-aldosterone system is stimulated in infants by a low sodium intake. A second stimulus was observed in the influence of the hypothalamo-neurohypophyseal system, when the plasma renin activity was suppressed by administration of antidiuretic hormone and sodium excretion increased due to a decreased aldosterone activity. Our study suggests that there exists a feedback between the renin-angiotensin-aldosterone system and ADH release and that this feedback plays an important role in the regulation of water and electrolyte balance in the young infant.
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PMID:Effects of ADH on the activity and function of the renin-angiotensin-aldosterone system in infants and in children. 93 34

Clinical states with portal venous hypertension are frequently associated with impairment in renal hemodynamics and water excretion, as well as increased renin secretion. In the present investigation, portal venous pressure (PVP) was increased in anesthetized dogs undergoing a water diuresis. Renal arterial pressure was maintained constant in all studies. As PVP was increased from 6 to 20 mm Hg, decreases in cardiac output (2.5-2.0 liter/min, P less than 0.05) and mean arterial pressure (140-131 mm Hg, P less than 0.05) were observed. Increases in PVP were also associated with decreases in glomerular filtration rate (GFR, 40-31 ml/min, P less than 0.001), renal blood flow (RBF, 276-193 ml/min, P less than 0.001), and increases in renin secretion (232-939 U/min, P less than 0.025) in innervated kidneys. No significant change in either GFR or RBF and a decrease in renin secretion occurred with increases in PVP in denervated kidneys. To dissociate the changes in cardiac output and mean arterial pressure induced by increase PVP from the observed decreases in GFR and RBF, studies were performed on animals undergoing constriction of the thoracic inferior vena cava. In these studies, similar decreases in cardiac output and mean arterial pressure were not associated with significant changes in GFR or RBF. Increases in PVP also were associated with an antidiuresis as urine osmolality increased from 101 to 446 mosmol/kg H2O (P less than 0.001). This antidiuresis was significantly blunted but not abolished by acute hypophysectomy. In hypophysectomized animals, changes in free water clearance and urine flow were linearly correlated as PVP was increased. These studies indicate that increases in PVP result in decreases in GFR and RBF and increases in renin secretion mediated by increased renal adrenergic tone. Increased PVP is also associated with antidiuresis; this antidiuresis is mediated both by vasopressin release and by diminished tubular fluid delivery to the distal nephron.
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PMID:Mechanisms of portal hypertension-induced alterations in renal hemodynamics, renal water excretion, and renin secretion. 96 99


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