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)

The purpose of the present study is to determine whether DOCA-salt treatment could cause an elevation of Na concentration of cerebrospinal fluid (CSF), which may increase blood pressure (BP) as a result of enhanced activity of sympathetic nervous system (SNS) and vasopressin (AVP). Blood pressure was gradually increased by DOCA-salt treatment. Serum NA was also elevated with time by DOCA-salt, and significantly higher in DOCA rats on the 4th treatment week, as compared with controls. By contrast, DOCA-salt did not alter CSF Na at any time of treatment. No relationship was detected between BP and CSF Na at any stage of DOCA-salt hypertension. The precent fall in BP by AVP antagonist or hexamethonium was always greater in DOCA-treated rats than that in the controls. These hypotensive effects were gradually, but consistently enhanced with the development of hypertension in DOCA rats. It is concluded that the enhanced activity of both SNS and AVP system responsible for DOCA-salt hypertension may be attributed to the mechanism(s) unrelated to the increased CSF Na concentration.
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PMID:Lack of increase in sodium concentration of cerebrospinal fluid in DOCA-salt hypertensive rats. 341 8

The antihypertensive effect of blockade of the brain renin-angiotensin system (brain RAS) was investigated in DOCA (deoxycorticosterone acetate)-salt hypertensive rats. Continuous intracerebroventricular (ICV) administration of SQ14225 (SQ; 1.25 micrograms X 0.5 microliter-1 X h-1) for 7 days attenuated the increase in blood pressure (99 +/- 5 vs. 116 +/- 4 mmHg on the 7th day) and also reduced the elevation of blood pressure (157 +/- 7 vs. 138 +/- 6 mmHg) in these hypertensive rats. Attenuation of increasing blood pressure in the developing phase following ICV SQ treatment was accompanied by decrease of fluid intake and prevention of elevation of the plasma vasopressin. In the established phase, in addition to reduction of the plasma vasopressin and decrease of fluid intake, restoration of the impaired baroreceptor reflexes was brought about by ICV SQ treatment. These results indicate that the brain RAS strongly influences the regulation of blood pressure in DOCA-salt hypertensive rats and that its mechanism of action is closely related to changes in sodium excretion, vasopressin, and the baroreceptor reflexes.
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PMID:Central renin-angiotensin system and the pathogenesis of DOCA-salt hypertension in rats. 352 27

1. The role of the sympathetic nervous system and the effect of vasopressin (AVP) on the hypotensive action of nifedipine (Nf) were evaluated in conscious, unrestrained normotensive and DOCA-salt hypertensive rats. 2. The hypotensive response to Nf was much greater in DOCA rats than in the controls. 3. Solitary blockade of the sympathetic nervous system or AVP, did not alter the Nf effect in either DOCA or control rats. However, a combination clearly diminished the effect of Nf in the DOCA group, but enhanced it in the controls. The inhibition of angiotensin II (ANG II) augmented the hypotensive effect of Nf in control animals, but not in the DOCA rats. The percentage fall in blood pressure with Nf was much the same in both groups after the combined inhibition of the sympathetic nervous system and AVP. 4. The enhanced hypotensive action of Nf in DOCA rats may be dependent on the hyperactivity of the sympathetic nervous system and AVP, which facilitates calcium influx, and in the normotensive animals the depressor response to Nf may relate to blockade of the calcium influx, independent of the sympathetic nervous system, AVP and ANG II.
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PMID:Influence of the sympathetic nervous system and vasopressin on the blood pressure lowering effect of nifedipine in deoxycorticosterone acetate-salt hypertensive rats. 365 32

Oral administration of the angiotensin I-converting enzyme inhibitor captopril produced a substantial reduction of blood pressure in DOCA-salt hypertensive rats. After oral administration of captopril (30 mg/kg), mean blood pressure decreased from 172 +/- 11 to 148 +/- 9 mmHg (P less than 0.01) in one hour and its antihypertensive effects lasted for the next seven hours. Plasma vasopressin levels showed a marked elevation in DOCA-salt hypertensive rats compared with control values (22 +/- 5 versus 5 +/- 3 pg/ml). This increase in vasopressin was significantly reduced by captopril from 25 +/- 5 to 8 +/- 6 pg/ml. In addition, whole body vascular reactivity to norepinephrine was examined. Responsiveness was at first attenuated but returned to control value in spite of reduction of both plasma vasopressin and blood pressure. Thus, captopril reduces blood pressure in DOCA-salt hypertensive rats and the fall in blood pressure is accompanied by reduction of plasma vasopressin and attenuation of vascular reactivity.
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PMID:Depressor effects of captopril in DOCA-salt hypertensive rats: role of vasopressin. 389 13

In the present study, deoxycorticosterone (DOC) and salt was administered to Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) by using silicone-rubber implants (DOC acetate, 100 mg/kg) and 0.9% NaCl as drinking water. SHR treated with DOC-salt for 4 weeks showed the characteristics of malignant hypertension including marked increases in blood pressure and left ventricular weight with typical histological changes in the kidney. DOC-salt treatment increased plasma vasopressin levels in WKY (from 6.1 +/- 0.5 to 8.9 +/- 0.8 pmol/l) but significantly more in SHR (from 5.0 +/- 0.6 to 15.8 +/- 1.2 pmol/l). Intravenous administration of the specific antagonist to the pressor effect of vasopressin, d(CH2)5Tyr(Me)AVP (10 micrograms/kg), decreased mean arterial pressure of DOC-salt treated WKY and SHR by 6.6 +/- 0.9 mmHg (P less than 0.05) and 9.7 +/- 1.7 mmHg (P less than 0.05) respectively. DOC-water treatment also increased plasma AVP levels in SHR to 10.5 +/- 0.8 pmol/l, but the vasopressin antagonist had little effect on blood pressure in these rats. Plasma levels of vasopressin were significantly correlated with both mean arterial pressure (r = 0.64) and left ventricular weight (r = 0.74). This suggests a close relationship between plasma AVP and severity of hypertension. The results of the present experiment demonstrate that vasopressin is part of the overall pressor mechanism which contributes to the maintenance of blood pressure in DOC-salt induced malignant hypertension in SHR, but the small fall in pressure produced by the AVP antagonists suggests that the contribution is of only minor importance.
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PMID:Contribution of vasopressin to the maintenance of blood pressure in deoxycorticosterone-salt induced malignant hypertension in spontaneously hypertensive rats. 395 9

The two major biological actions of vasopressin are antidiuresis and vasoconstriction. The antidiuretic action of low concentrations of vasopressin is well established and concentrations 10 to 100 times above those required for antidiuresis elevate arterial blood pressure. Antidiuresis is mediated by V2-receptors at the kidney, whereas vasopressin constricts arterioles by binding at V1-receptors. Pharmacological effects of specific antagonists of the vasoconstrictor activity of vasopressin (vascular or V1-receptor antagonists) are presented. Low concentrations of vasopressin do have significant hemodynamic effects. Physiological concentrations of vasopressin cause vasoconstriction and elevate systemic vascular resistance. In subjects with intact cardiovascular reflex activity, however, cardiac output falls concomitantly and blood pressure therefore does not change. In animals with baroreceptor deafferentation or in patients with blunted baroreceptor reflexes (autonomic insufficiency) a rise in plasma vasopressin causes vasoconstriction and an increase in blood pressure, because cardiac output does not fall under these conditions. Vasopressin contributes substantially via increase in systemic vascular resistance to maintain blood pressure during water deprivation. During hemorrhage and hypotension vasopressin has a major role to restore blood pressure. In experimental hypertension vasopressin contributes to the development and maintenance of high blood pressure in DOCA, but not in genetic hypertensive rats. The role of vasopressin in human hypertension is not yet clear. Vasopressin in extrahypothalamic areas of the brain affects circulatory regulation by interaction with central cardiovascular control centers. The exact mechanism of how vasopressin is involved in central regulation of blood pressure remains to be established. In contrast to our previous opinion vasopressin is a vasoactive hormone also at low plasma concentrations. Its cardiovascular action is more complex than previously assumed.
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PMID:[Cardiovascular effect of the antidiuretic hormone arginine vasopressin]. 406 6

The response of trained, conscious dogs to an acute water load was studied before adrenalectomy and under five conditions of hormonal replacement and sodium intake after adrenalectomy. Before adrenalectomy, with the dogs drinking isotonic saline, the minimal urinary osmolality (Uosm) was 47+/-7 (SEM) mOsm and free-water clearance (C(H2O)) was 8.6+/-1 ml/min. These values were not different after adrenalectomy with or without deoxycorticosterone (DOCA) if the animals continued to drink saline and receive dexamethasone. Moreover, after adrenalectomy in the presence of saline drinking both dexamethasone and DOCA could be withdrawn for up to 4 days without impairment of diluting ability (Uosm, 54+/-7 mOsm and C(H2O), 7.3+/-1 ml/min). In contrast, when the dogs drank tap water (Na intake 30 mEq/day), water loading in the absence of dexamethasone and DOCA was associated with a significantly higher Uosm (127+/-28 mOsm) and lower C(H2O) (2.7+/-0.3 ml/min). Replacing DOCA alone in the presence of this limited Na intake returned diluting ability to normal (Uosm 31+/-7 mOsm, C(H2O) 7.7+/-0.5 ml/min). Glomerular filtration rate for each animal was the same under each condition except for a significant diminution which occurred when dexamethasone and DOCA were withdrawn while the animals were on a 30 mEq sodium intake. In contrast to previous conclusions, the present results indicate that in the absence of adrenal hormones normal renal diluting ability may occur, indicating both maximal suppression of vasopressin release and maximal distal tubular impermeability to water. In the present study the diluting defect observed after adrenalectomy related to negative sodium balance and could be overcome by either replacement with DOCA or a high intake of sodium alone.
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PMID:Importance of sodium intake and mineralocorticoid hormone in the impaired water excretion in adrenal insufficiency. 503 19

Effect of chronic angiotensin converting enzyme blockade on the pressor response to exogenous angiotensin II, noradrenaline and vasopressin were evaluated in DOCA-salt induced hypertensive rats using teprotide. The blood pressure of rats receiving teprotide chronically was reduced markedly. The pressor responses to exogenous angiotensin II was accentuated, while that of noradrenaline and vasopressin were significantly reduced. It is concluded that besides the angiotensin converting enzyme blocking action, the decrease in sensitivity of the pressor response to noradrenaline and vasopressin may contribute towards the antihypertensive activity of teprotide given chronically.
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PMID:Effect of chronic angiotensin-converting enzyme blockade on pressor responses to exogenous angiotensin II, noradrenaline and vasopressin in deoxycorticosterone acetate salt (DOCA)-induced hypertensive rats. 609 11

Hypothalamic and neurophypophyseal levels of catecholamines and peptides were measured in spontaneous and deoxycorticosterone (DOCA)/salt hypertension. Catecholamines, norepinephrine, epinephrine and dopamine were measured by electrochemical detection while the peptides, vasopressin, oxytocin, luteinizing hormone-releasing hormone (LHRH), the enkephalins and somatostatin (SRIF) were measured by radioimmunoassay. Blood pressure was significantly elevated in both groups as compared to their controls. Marked changes in central neural peptides were observed in the SHR, while no differences were seen in DOCA/salt hypertension. Hypothalamic vasopressin, oxytocin, LHRH and SRIF were significantly decreased. In the posterior pituitary, enkephalins were increased twofold in the SHR. With regard to catecholamines, there was no change in hypothalamic content. However, a dramatic decrease in neurohypophyseal dopamine was observed in SHR. Plasma levels of vasopressin were significantly elevated in both types of hypertension while oxytocin was increased only in the DOCA/salt model. These result show that (1) a wide spectrum of neuroendocrine changes are associated with genetic hypertension, (2) there are CNS differences between DOCA/salt and spontaneous hypertension, and (3) central aminergic changes may be involved in th neuroendocrine alterations seen in the SHR.
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PMID:Central neural peptides and catecholamines in spontaneous and DOCA/salt hypertension. 611 62

The mechanism of the hypotensive effect of 1-O-octadecyl-2-O-acetyl-glycero-3-phosphorylcholine (C18- AGPC ) was examined. Synthetic C18- AGPC caused dose-dependent hypotension in conscious rats. The activity was almost the same in DOCA and renal hypertensive rats. This suggests that it is not a renin inhibitor. Hypotension also appeared in pithed rats. This suggests that the effect is not due to a central mechanism. Hypotension did not result from platelet aggregation or bronchial constriction. Since C18- AGPC suppressed not only the pressor response to noradrenaline but also to angiotensin II and vasopressin, and furthermore, did not disturb the dose-response curve of noradrenaline in the isolated aorta, the possibility of the agent being an alpha-adrenergic antagonist is ruled out. In the PGF2 alpha-contracted rat aorta. C18- AGPC caused marked vasodilation, which disappeared after removal of the endothelium. Perfusion pressure decreased in the blood-perfused rat hindquarters but not in the Tyrode solution-perfused ones. C18- AGPC induced a positive inotropic effect in isolated rat atrium. The hypotensive effect of synthetic C18- AGPC seems to be mainly due to endothelium-dependent vasodilation.
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PMID:Mechanism(s) of the hypotensive effect of synthetic 1-O-octadecyl-2-O-acetyl-glycero-3-phosphorylcholine. 614 57


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