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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The specific vasopressin receptor of V1 vascular subtype, which mediates platelet aggregation, has been found on human platelets. We investigated the binding characteristics using tritiated arginine vasopressin [3H]-AVP and platelet aggregation with AVP turbidometrically in normal subjects, patients with WHO class II essential hypertension and patients with malignant-phase hypertension. In essential hypertensives Bmax was significantly higher than that in normal subjects, but there were no differences in affinity and the maximal percentage aggregation between them. In malignant-phase hypertensives Bmax and maximal percentage aggregation were significantly lower than those in normals and essential hypertensives, although there was no difference in the affinity between them. With radio-immunoassay, the mean platelet-free plasma AVP level was significantly higher in malignant-phase hypertensives than those in normals and essential hypertensives, whereas there was no difference in mean platelet AVP levels between them. In essential hypertensives Bmax and maximal percentage aggregation did not change, but in malignant-phase hypertensives Bmax increased significantly and maximal percentage aggregation tended to normalize after treatment.
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PMID:Platelet vasopressin receptor in essential hypertension. 297 78

The contribution of vasopressin and angiotensin II to the maintenance of blood pressure after short-term autonomic blockade was investigated in conscious Long-Evans and Brattleboro (vasopressin-deficient; hereditary diabetes insipidus) rats. After short-term autonomic blockade by atropine (1 mg/kg), propranolol (5 mg/kg), and pentolinium (5 mg/kg and 10 mg/kg/hr), the fall in blood pressure was significantly greater in Brattleboro rats than in Long-Evans rats (48 +/- 3 vs 32 +/- 2 mm Hg; p less than 0.01). Administration of the vasopressin vascular receptor antagonist D(CH2)5Tyr-(Me)AVP (2 micrograms/kg) caused further blood pressure decreases only in Long-Evans rats, so that the final blood pressure in both groups was identical. Administration of enalaprilat (10 mg/kg), an angiotensin converting enzyme inhibitor, further reduced blood pressure in both strains. When enalaprilat was given first after autonomic blockade, it reduced blood pressure in Brattleboro rats but not in Long-Evans rats. Administration of the vasopressin antagonist after enalaprilat further reduced blood pressure only in Long-Evans rats. The fall in blood pressure following vasopressin blockade was greater than that occurring after angiotensin converting enzyme inhibition (14 +/- 1 vs 6 +/- 1 mm Hg; p less than 0.05) in autonomic blockade Long-Evans rats. Plasma levels of vasopressin in Long-Evans rats increased markedly after short-term autonomic blockade, whereas plasma renin and angiotensin II levels were unchanged. Plasma angiotensin II levels were increased by the vasopressin antagonist and decreased by enalaprilat. We conclude that, due to sympathetic nervous system blockade and consequent blunting of renal renin release, vasopressin has a greater capacity than the renin-angiotensin system for maintaining blood pressure after short-term autonomic blockade.
Hypertension
PMID:The contribution of vasopressin and angiotensin to the maintenance of blood pressure after autonomic blockade. 298 71

Lesions of the ventrolateral medulla of the rabbit, coinciding with the A1 noradrenaline cell bodies (A1 lesions) produced fortyfold increases in the plasma levels of vasopressin and adrenaline, a twofold increase in plasma noradrenaline and a substantial increase in plasma renin activity. These increases accompanied the hypertension and bradycardia that follow A1 lesions. The vasoconstriction and hypertension were completely abolished by phentolamine, an alpha-adrenoceptor antagonist, when it was administered before lesions and were markedly reduced when it was given after lesions. On the other hand, administration of an antagonist to the vasoconstrictor action of vasopressin (d(CH2)5Tyr(Me)AVP) or an angiotensin converting enzyme inhibitor had little effect. Prior removal of the adrenal glands prevented any rise in plasma adrenaline levels but had no effect on the pressure response to subsequent A1 lesions. These results indicate that the vasoconstriction and hypertension were predominantly mediated by alpha-adrenoceptor stimulation, acting mainly through sympathetic vasoconstrictor nerves. The fall in heart rate following A1 lesions was approximately halved by pretreatment either with d(CH2)5Tyr(Me)AVP alone, or by blockade of the vagus and sympathetic with scopolamine and propranolol; it was completely abolished by combined pretreatment with all three agents. The experiments show that vasopressin release makes a major contribution to the bradycardia acting at least in part through mechanisms that are independent of cardiac vagal or sympathetic nerves.
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PMID:The mechanism of hypertension and bradycardia following lesions of the caudal ventrolateral medulla in the rabbit: the role of sympathetic nerves, circulating adrenaline, vasopressin and renin. 299 15

To determine the role of endogenous vasopressin (AVP) in cardiovascular response to central alpha-adrenoceptor stimulation, alpha 1-agonist methoxamine or alpha 2-agonist clonidine was administered intracerebroventricularly (ICV) to conscious Long-Evans (LE) rats as well as Brattleboro rats with hereditary hypothalamic diabetes insipidus (DI). In LE rats, ICV methoxamine increased blood pressure (BP) and decreased heart rate (HR), while ICV clonidine caused initial hypertension associated with bradycardia followed by prolonged hypotension with tachycardia. In DI rats, however, ICV methoxamine had no detectable effect on BP and HR, whereas ICV clonidine produced greater hypotension than in LE rats together with less initial bradycardia. Plasma levels of AVP increased 5-15 fold by methoxamine but did not change by clonidine. The intravenous (IV) but not ICV pretreatment with AVP vascular receptor antagonist d (CH2)5 Tyr (Me) AVP significantly attenuated the cardiovascular effects of methoxamine in LE rat, while neither IV nor ICV pretreatment with AVP antagonist modulated the cardiovascular effects of clonidine. These results provide the evidence for the implication of endogenous AVP in the cardiovascular response to central stimulation of alpha-adrenoceptors.
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PMID:Evidence for the implication of endogenous vasopressin in cardiovascular response to central alpha-adrenoceptor stimulation. 302 47

Recent interest has focused on the role of vasopressin (AVP) in blood pressure (BP) regulation. This study was performed to determine if vasopressin has a compensatory pressor role following acute diuresis in both normal rats and in rats with subtotal nephrectomy (SN) or in rats with SN-salt induced hypertension. An inhibitor (AVP-I), specific for the AVP vascular smooth muscle receptor, was administered intravenously to assess the AVP dependency of the BP. Furosemide administration significantly increased plasma AVP levels in all rats. Administration of AVP-I did not change BP in the normal rats with or without prior furosemide administration or in the SN rats without furosemide administration. In contrast, after furosemide administration, AVP-I significantly decreased mean BP in the SN rats. The administration of AVP-I to the SN-salt hypertensive rats, with or without furosemide administration, significantly decreased mean BP. In conclusion, AVP has a compensatory pressor role in SN rats after acute diuresis, with or without salt-induced hypertension, but not in the normal rat.
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PMID:Compensatory pressor role of vasopressin following acute diuresis. 318 69

We evaluated whether or not increased sodium (Na) concentrations of cerebrospinal fluid (CSF) and stimulated activities of brain renin-angiotensin system (RAS) contribute to an enhanced hypertension by salt overload in spontaneously hypertensive rats (SHR). Long-term salt loading (1% NaCl solution as drinking fluid) accelerated the development of hypertension in SHR, but did not alter the blood pressure (BP) in normotensive Wistar-Kyoto rats (WKY). CSF Na concentration was elevated in uninephrectomized (Nx) group as compared to that in control SHR, while in WKY CSF Na was not influenced by the treatment. A fall in BP by intravenous AVP antagonist or hexamethonium was greater in salt-loaded SHR than in controls. This hypotensive response to the combined blockade of AVP and SNS correlated with CSF Na in SHR but not in WKY. Plasma concentration of AVP and epinephrine tended to increase in relation to the degree of salt loading in SHR but not in WKY. Pressor responses to intracerebroventricular (ICV) angiotensin II (AII) and NaCl were greater in SHR than in WKY, although these responses were not influenced by chronic salt load in either SHR or WKY. The enhanced hypertensive action of ICV NaCl in SHR was abolished by pretreatment with ICV AII antagonist. Chronic saline drinking enhanced the depressor effect of ICV captopril in SHR but not in WKY. These observations suggest that salt overload in SHR may cause an elevated CSF Na concentration and an enhanced activity of brain RAS, which may increase activity of SNS and release of AVP, resulting in an enhanced development of hypertension.
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PMID:Central and peripheral mechanisms of the enhanced hypertension following long-term salt loading in spontaneously hypertensive rats. 322 97

In order to understand the regulation of vascular vasopressin receptors in hypertension, vasopressin (AVP) binding sites and the pressor response to AVP in the perfused mesenteric vasculature of DOCA-salt hypertensive rats, sodium-loaded and DOCA-treated rats were investigated. The binding capacity for AVP (Bmax) was significantly reduced (P less than 0.05) in uninephrectomized, DOCA-treated rats (70 +/- 17 fmol/mg protein) and in DOCA-salt hypertensive rats (90 +/- 9 fmol/mg protein) with respect to uninephrectomized rats (130 +/- 32 fmol/mg protein) or uninephrectomized salt-loaded rats (155 +/- 47 fmol/mg protein), with no change in affinity. In these rats with lower receptor density, however, the maximal pressor response to AVP in the perfused mesenteric vascular bed was increased (P less than 0.05). In DOCA-salt hypertensive rats plasma AVP was higher than in the other groups. In similarly treated rats with intact kidneys, which therefore did not become hypertensive, receptor density was significantly decreased after combined DOCA-salt treatment, together with an exaggerated pressor response to AVP and increased plasma AVP concentrations. These results suggest that AVP receptors are down-regulated when there is an increment in the plasma concentration of AVP, although other factors may also play a role. Biological responses to AVP are, however, increased in spite of decreased receptor density and this phenomenon is independent of the elevation in blood pressure and results from an exaggerated response mediated by post-receptor mechanisms.
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PMID:Vascular binding sites and biological activity of vasopressin in DOCA-salt hypertensive rats. 328 26

The features of hypertension produced in the rat by chemical medullectomy with 2-bromoethylamine hydrobromide are described. This procedure partially prevents the fall in blood pressure that occurs when the constriction is removed from the renal artery of rats with two-kidney one-clip Goldblatt hypertension. In normal rats, chemical medullectomy causes a moderate but consistent blood pressure elevation that is dose related and associated with elevation of peripheral resistance; the venous side of the circulation is normal. The hypertension is not associated with sodium retention or with activation of the renin angiotensin system. Although vasopressin levels are elevated, the rise is only modest, and blood pressure is not reduced by a vascular AVP antagonist. It is concluded that chemical medullectomy removes the source of a humoral substance that has been shown by other workers to carry out a vasodepressor role. The chemical medullectomy model therefore offers new insights into the renomedullary vasodepressor system.
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PMID:Renal vasodepressor mechanism: characterization by chemical medullectomy. 328 47

Our previous finding that dexamethasone-induced hypertension in rats is associated with enhanced reactivity of mesenteric arteries to arginine vasopressin but not to angiotensin II (Ang II) or norepinephrine has led us to postulate that vasopressin contributes to the development or maintenance of glucocorticoid-induced hypertension. To test this view, we investigated the effects of vasopressin, Ang II, norepinephrine, and the vasopressin V1 receptor antagonist d(CH2)5Tyr(Me)AVP on mean arterial blood pressure and heart rate with and without ganglionic blockade with hexamethonium and angiotensin I (Ang I) converting enzyme inhibition with MK 421 in pentobarbital-anesthetized rats made hypertensive by treatment with dexamethasone (1.8 mg/kg/wk for 14 days). Administration of vasopressin, Ang II, or norepinephrine (0.003-3 microgram i.v.) produced a dose-related increase in arterial blood pressure. The pressor response to vasopressin, but not to Ang II or norepinephrine, was greater in dexamethasone-treated than in vehicle-treated animals, and this difference became more pronounced in rats that received hexamethonium and MK 421. Administration of the vasopressin V1 receptor antagonist d(CH2)5Tyr(Me)AVP significantly reduced arterial pressure in dexamethasone-treated but not in vehicle-treated animals. Hexamethonium and MK 421 reduced arterial blood pressure in dexamethasone-treated as well as in vehicle-treated rats; however, arterial blood pressure remained higher in the former. Administration of the vasopressin V1 receptor antagonist produced a greater reduction in arterial blood pressure in dexamethasone-treated than in vehicle-treated rats. These data suggest that vasopressin contributes to glucocorticoid-induced hypertension, which is probably due to enhanced vascular reactivity to the peptide.
Hypertension 1988 Feb
PMID:Contribution of vasopressin in dexamethasone-induced hypertension in rats. 334 65

The acute effects of physiological levels of AVP and oxytocin administration on renal water and sodium handling have been investigated in New Zealand genetically hypertensive and normotensive rats. AVP infusion was associated with an antidiuresis in both normotensive and hypertensive rats and while normotensive rats also displayed a dose-related natriuresis, this was attenuated in hypertensive rats. Oxytocin administration had no effect on urine flow or sodium excretion in normotensive rats, but was associated with an antidiuresis in hypertensive rats. Combined hormone infusion produced a greater reduction in urine flow than following AVP alone in both normotensive and hypertensive groups and was associated with a potentiation of the natriuretic action of AVP in the hypertensive animals. The data suggest that the contribution of oxytocin to renal sodium excretion in hypertensive rats may be suppressed. A compensatory increase in basal AVP secretion in hypertensive rats may overcome their apparent renal insensitivity to AVP, to maintain appropriate sodium excretion. This intriguing disturbance in neurohypophysial function may reflect or possibly contribute to the hypertension of these animals.
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PMID:Neurohypophysial hormone influence on renal function in the New Zealand genetically hypertensive rat. 339 74


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