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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A central stimulatory effect of angiotensin II (AII) on the secretion of arginine-vasopressin (AVP) has been described. The competitive blocker of AII, saralasin (SAR) has been used for diagnostic purposes in angiotensin-dependent hypertension. In addition SAR has a partially agnoistic effect. The aim of the present study was to demonstrate whether AVP-levels can be influenced during SAR-induced renin stimulation. In 9 patients with essential hypertension blood pressure dropped significantly under SAR (10 microgram/kg/min over a 30 min period). Before and after SAR plasma renin activity (PRA) and AVP were measured by RIA, SAR evoked significantly increments of PRA in all patients and of AVP in 6 patients. The increased serum concentrations of AVP following SAR may be explained either by the depressor effect of SAR, its diminished concentration at the central receptor, or a partial AII-agonistic effect.
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PMID:[Effect of saralasin on plasma renin activity and arginine-vasopressin in patients with angiotensin-dependent hypertension (author's transl)]. 68 28

1. Hepatic elimination of renin was measured in 10 well-compensated cardiac patients with normal liver function during a control period and during a period of reduced hepatic plasma flow, induced by physical exercise (seven patients) or intravenous infusion of lysine vasopressin (three patients). 2. Hepatic renin elimination rate (hepatic plasma flow x arterial-hepatic vein difference of plasma renin activity) was found to be linearly correlated with arterial plasma renin activity (r = 0.986, P less than 0.001). 3. When hepatic plasma flow fell by 45% the hepatic extraction ratio of renin (arterial-hepatic vein plasma renin activity difference/arterial plasma renin activity) increased by 75%. Hepatic renin clearance (hepatic plasma flow x extraction ratio) remained constant. 4. The results indicate that changes in the hepatic elimination rate of renin do not contribute to changes in plasma renin activity during these events.
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PMID:Hepatic elimination of renin in man. 71 52

Isoproterenol is a potent dipsogen and antidiuretic agent. It also stimulates the release of renin from the kidney. Evidence is presented to substantiate the view that the drinking and increased vasopressin release that follow the systemic injection of a small dose of isoproterenol are mediated via increased activity of the renin-angiotensin system. Larger doses of isoproterenol, which have profound effects on the cardiovascular system, cause drinking and vasopressin release by mechanisms that do not depend solely on the renin-angiotensin system. Other experiments discussed do not support the hypothesis that hypothalamic beta-adrenergic neurons are important in facilitating thirst. Low doses of isoproterenol are more effective in causing drinking and vasopressin release when given peripherally rather than centrally. Evidence is discussed that supports the view that isoproterenol given centrally leaks into the periphery and causes release of renin and subsequent stimulation of drinking and vasopressin release.
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PMID:Beta-adrenergic thirst and its relation to the renin-angiotensin system. 71 May 89

Cerebral lesions involving most of the anterior wall of the ventricle, and the medial part of the septal region, induced a permanent loss of thirst in two goats. The ventral part of the lamina terminalis remained intact in one of the animals. Pronounced dehydration (10--13% loss of b.wt.) developed during periods (3--7 days) when water supplementation was omitted. Determinations of plasma arginine vasopressin in one of the animals revealed that the dehydration did not cause any significant increase in the secretion of antidiuretic hormone. However, the water deficit induced a considerable rise in plasma renin activity and tachycardia. If anything, the caroitid blood pressure became slightly elevated towards the end of 7 d dehydration periods. The lesions obviously inactivated a cerebral sensory mechanism controlling water balance. It may have been due mainly to destruction of juxtaventricular receptors in the anterior hypothalamic region, but perhaps also to a disruption of afferents from such receptors located posterior to this cerebral level.
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PMID:A study of permanent adipsia induced by medial forebrain lesions. 71 67

Studies on the vasopressor role of the antidiuretic hormone arginine-vasopressin (AVP) in DOC hypertension, in two-kidney Goldblatt hypertension, and in spontaneous hypertension of rats, and during acute blood pressure elevation after intracerebroventricular injection of angiotensin II and in glycerol-induced acute renal failure of rats are reviewed. For the measurement of plasma AVP a radioimmunoassay has been developed. For this assay, a series of criteria has been met which allows the conclusion that, in plasma of rats, the antibody measures AVP only. For the blockade of vasopressor effects of AVP a specific antiserum has been used. On the basis of a series of control studies it has been concluded, but not proven that the antiserum lowers blood pressure exclusively by blockade of AVP. It could be shown that in the various animal models of hypertension and of acute blood pressure elevation AVP exerts systemic vasoconstriction when its plasma concentrations are elevated. In those models where the renin-angiotensin system played no role in blood pressure control, the height of blood pressure was closely related to the plasma AVP concentrations. When this relationship was compared with that obtained after the i.v. infusion or injection of AVP, a marked shift to the left became apparent. Hence, sensitization to the vasopressor effect of AVP had occurred, the factor of sensitization amounting to more than 1,000. It is concluded that AVP is not only an antidiuretic hormone but also a vasopressor hormone, and that any systemic vasopressor effect of AVP requires a mechanism of sensitization.
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PMID:Neurohypophyseal vasopressor principle: vasopressor hormone as well as antidiuretic hormone? 73 54

1. Blood pressure is controlled by both integrated neurogenic and humoral vasoactive mechanisms. 2. Both vasopressor (angiotensin and vasopressin) and vasodepressor (bradykinin) hormonal peptides have been identified. 3. In acute experimental renal hypertension in the rat plasma renin, angiotensin and vasopressin have all been shown to be elevated. 4. Associated with this increase in vasopressor hormonal peptides, urinary kallikrein excretion has been demonstrated to be reduced during the development of renal hypertension. 5. The level of blood pressure achieved in experimental renal hypertension is probably a summation of these vasoactive peptides as well as other factors.
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PMID:Vasoactive peptides in experimental renal hypertension. 73 55

This study was carried out to assess the influence of saralasin (SAR), an angiotensin II-analogue, on peripheral and central angiotensin II-receptors by measurements of plasma renin activity (PRA) and arginine-vasopressin (AVP) release. Before and during i.v. infusion of 10 microgram/kg/min of SAR over a 30 minute period, blood samples were obtained from 15 recumbent hypertensive patients (7 renovascular, 8 essential) to determine hormone activities by radioimmunoassay. In 10 patients with a decrease of blood pressure following SAR, PRA increased significantly whereas AVP levels increased significantly in only 7 of these patients. In the remaining 5 patients without a fall of blood pressure, PRA and AVP remained virtually unchanged. The results indicate that an enhanced AVP release may be due to a hypotensive stimulus induced by SAR in angiotensinogenic hypertension. A direct influence of SAR on central receptors is unlikely under the conditions studied.
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PMID:Effect of saralasin on plasma renin activity and arginine-vasopressin in hypertensive man. 74 Jun 74

The effect of isoproterenol (6 microgram/kg sc) on drinking, urine flow, and vasopressin secretion was examined in a group of trained dogs with chronically implanted third ventricular cannulae. Isoproterenol stimulated drinking in association with a reduction in urine flow and an increase in urine to plasma osmolality ratio. Plasma renin activity increased from 3.1 +/- 0.8 to 13.0 +/- 2.7 ng/ml/3 h and plasma vasopressin concentration increased from 11.3 +/- 1.3 to 40.3 +/- 12.5 pg/ml. The effect of isoproterenol was reexamined during an intracerebroventricular infusion of the angiotensin II antagonist, saralasin (0.02 microgram/kg/min). This treatment did not affect the isoproterenol-induced increase in plasma renin activity, but inhibited the drinking, antidiuresis, and increase in plasma vasopressin concentration. These data indicate that the effects of isoproterenol on drinking, urine flow, and vasopressin secretion are mediated via the renin-angiotensin system.
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PMID:Evidence that the effects of isoproterenol on water intake and vasopressin secretion are mediated by angiotensin. 74 84

Sodium excretion is correlated with kallikrein excretion in man, rabbits and rats on a free sodium and water intake, but not on a constant sodium or constant water intake. The correlation also exists during arterial infusion of angiotensin II, substance P and various vasodilators. During sodium depletion, the stimulation of the renin-angiotensin system causes increased drinking in rats and rabbits. The high angiotensin levels would stimulate kallikrein excretion. The excretion of water and dilution of urine are facilitated by the renal kallikrein-kinin system, even when antidiuretic hormone is high. This negative correlation between urinary osmolality and kallikrein excretion exists during arterial infusion of angiotensin or substance P and various vasodilators. During renal artery constriction, the kallikrein release per minute decreases, but over successive 10-minute periods, the kallikrein concentration in urine rises. This rise is correlated with some recovery in the clearance of rho-aminohippurate and inulin. Since kallikrein is released into renal lymph during saline infusion at a rate that correlates with its release into the urine, it is suggested that the renal kallikrein-kinin system protects the renal vasculature against the constricting action of the renin-angiotensin system. The decreased release of kallikrein (via the lymphatics into the circulation) during renal artery constriction, or decreased renal compliance, would potentiate the hypertensive effect of these procedures which cause increased renin release.
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PMID:The renal kallikrein-kinin system and the regulation of salt and water excretion. 76 62

During the onset of malignant hypertension (MH) in rats treated with deoxycorticosterone trimethylacetate (DOC), plasma arginine vasopressin (AVP) concentrations increase tenfold as a consequence of hypovolemia and hyperosmolality. In benign hypertensive (BH) rats, plasma AVP is increased threefold in comparison with control animals. Plasma renin is markedly suppressed in both BH and MH animals. In MH rats, biologically active AVP antiserum lowers blood pressure (BP) transiently to normal or subnormal levels; in BH rats, a small BP-lowering effect of the AVP antiserum is seen. (Biologically active angiotensin II antiserum does not lower BP in MH rats.) The relationship between the height of BP and plasma AVP concentration in DOC hypertensive rats indicates, when compared with that relationship in diabetes insipidus rats infused with AVP, a marked enhancement of the vasopressor effect of AVP. These findings and the earlier observation of vasopressin-induced vascular damage by Byrom (F. B. Byrom, The Hypertensive Vascular Crisis. London: Heinemann, 1969) strongly suggest that ADH is involved as a vasopressor hormone in the pathogenesis of malignant DOC hypertension.
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PMID:Vasopressor role of ADH in the pathogenesis of malignant DOC hypertension. 84 73


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