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 intracerebroventricular injection of eledoisin (ELE), or of other tachykinins with potent agonist activity at neurokinin B (NK-3) receptors, increases plasma vasopressin in the rat. The effect is antagonized by saralasin pretreatment, thus suggesting that it is mediated by angiotensin receptor activation. Since the magnocellular part of the hypothalamic paraventricular nucleus (PVN) is very rich in NK-3 receptors, the present study was aimed at investigating the role of this nucleus in the effect of ELE on plasma vasopressin. Direct injection of ELE into the PVN increased plasma vasopressin levels more potently than the injection of the same doses into the lateral ventricle. Lesioning of the magnocellular part of the PVN completely abolished the increase in plasma vasopressin induced by the injection of ELE 100 ng/rat into the lateral ventricle. Pretreatment into the PVN either with saralasin or with captopril resulted in a marked suppression of the effect of ELE on plasma vasopressin. These findings indicate the PVN as a site of action for the central effect of tachykinins on plasma vasopressin and suggest that the angiotensin mediation of the effect might take place in the same nucleus.
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PMID:The hypothalamic paraventricular nucleus is a site of action for the central effect of tachykinins on plasma vasopressin. 201 11

The aim of this study was to investigate the action of the heptapeptide angiotensin-(1-7) on the spontaneous activity of paraventricular neurons using microiontophoresis. Recent immunocytochemical investigations have shown that this product of angiotensin I is predominantly located in cells and fibers of the forebrain and brain stem. Our results show that most neurons in the paraventricular nucleus are excited by angiotensin-(1-7) at a dose of 50-80 nA. In comparison with angiotensin II or angiotensin III, the onset of response and the occurrence of the maximal effect were significantly delayed. With higher doses of angiotensin-(1-7), there was a decrease in latency and a dose-dependent increase in firing frequency. Of all the angiotensin compounds tested, angiotensin III was the most potent. Preliminary results obtained with an angiotensin antagonist show that the action of angiotensin II, angiotensin III, and angiotensin-(1-7) is blocked by the angiotensin receptor subtype 2 antagonist CGP 42112A. Because the angiotensin-(1-7) system in the brain is associated with central vasopressinergic pathways, vasopressin was tested in a similar way. Neurons in the paraventricular nucleus that were excited by iontophoretically applied angiotensins showed a weak response to vasopressin. Occasionally, a small excitatory action was observed. Our results support the hypothesis that the heptapeptide angiotensin-(1-7) is a biologically active neuropeptide. The data also suggest that amino terminal fragments of angiotensin II are not inactive degradation products.
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PMID:Neurophysiological responses to angiotensin-(1-7). 204 57

In the pentobarbital sodium-anesthetized rat, dehydration for 24 h increased ion and water absorption from the jejunum. Dehydration also elevated plasma concentrations of angiotensin peptides and plasma renin activity but did not significantly alter plasma aldosterone concentrations. Infusion of tyramine, norepinephrine, and angiotensin II (AII) also stimulated jejunal absorption in a manner similar to dehydration. The elevation of jejunal absorption in response to dehydration is totally inhibited by the converting enzyme inhibitor captopril and the angiotensin receptor antagonist [lle7]AIII. Thus, increased jejunal absorption following dehydration is mediated by the renin-angiotensin system and is not secondary to either aldosterone or to antidiuretic hormone release. Further experiments demonstrated that the increase in jejunal absorption in response to dehydration was unaffected by propranolol but was totally abolished by phentolamine, prazosin, and peripheral sympathectomy. It is proposed that AII stimulates jejunal absorption by enhancing transepithelial transport processes and/or by altering the balance of Starling forces governing fluid absorption across enteric capillaries. Angiotensin thus appears to be a physiologically important mediator of jejunal absorption in states characterized by extracellular volume depletion.
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PMID:Modulation of jejunal ion and water absorption by endogenous angiotensin after dehydration. 674 21

1. In this article we review the physiological actions of the heptapeptide angiotensin-(1-7) [Ang-(1-7)] at the periphery and on central pathways involved in the control of arterial pressure. Peripherally Ang-(1-7) has been shown to present a potent antidiuretic effect on water-loaded rats. Microinjection of pmol amounts of Ang-(1-7) into the dorsomedial or ventrolateral medulla (VLM) of anesthetized rats produces cardiovascular effects comparable to Ang II. In addition, in vitro experiments have shown that Ang-(1-7) has a potent vasopressin and prostaglandin releasing activity and excites neuronal activity in the hypothalamus and medulla. 2. Evidence for the existence of a new angiotensin receptor subtype that mediates the central cardiovascular actions of this active peptide of the renin-angiotensin system (RAS) is also provided. Neither the AT1 receptor antagonist DUP 753 or the AT2 receptor antagonist CGP 42112A blocked the pressor response produced by microinjection of Ang-(1-7) into the rostral VLM. However, the effect of Ang-(1-7) on VLM was completely abolished by the non-specific angiotensin receptor antagonist, Sar1-Thr8-Ang II. 3. The data presented here reinforce the hypothesis of the existence of complex site-specific interactions between multiple angiotensins and multiple receptors in the mediation of important central and peripheral effects of the RAS.
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PMID:Central and peripheral actions of angiotensin-(1-7). 808 84

The roles of the sympathetic nervous system, angiotensin II, and arginine vasopressin in the cardiovascular-renal responses to nitric oxide synthesis inhibition were examined in eight conscious dogs equipped with arterial and venous catheters and a nonoccluding bladder catheter. Nitric oxide inhibition was achieved by intravenous infusion of NG-nitro-L-arginine methyl ester (L-NAME) at 37.1 nmol/kg per minute for 140 minutes in the control group. The same dogs, after a 1-week recovery, were pretreated for 2 days with either prazosin for alpha 1 blockade, prazosin plus propranolol for alpha 1 plus beta blockade, L-158,809 for angiotensin receptor blockade, or d(CH2)Tyr(Me)arginine vasopressin for vasopressin-V1 blockade, and the L-NAME infusion was repeated. After 140 minutes of L-NAME infusion into the control group, mean arterial pressure and renal vascular resistance had increased 16% and 71%, and renal blood flow, glomerular filtration rate, urine flow, and urinary sodium excretion had decreased 33%, 16%, 61%, and 64%, respectively. The decrement in renal blood flow and glomerular filtration during L-NAME administration was unaffected by any of the neurohumoral blockers. During V1 blockade L-NAME resulted in only a 3% increase in arterial pressure, attenuation of the renal vascular resistance response, and almost total elimination of the decrease in urine flow. During angiotensin blockade the L-NAME-induced increase in arterial pressure was markedly attenuated, and the decrease in urinary sodium excretion was attenuated in the alpha 1 plus beta blockade group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms involved in the cardiovascular-renal actions of nitric oxide inhibition. 820 34

Angiotensin II (Ang) injected intracerebroventricularly stimulates neurohypophyseal vasopressin (AVP) release into the peripheral circulation. As we have shown previously, central actions of Ang II in the rat forebrain are mediated by the AT1A receptor subtype. In the present paper, we attempted to clarify the cellular localization of the AT1A receptor mRNA in the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei, in order to reappraise the conflicting data on the nature of the angiotensin II receptor involved in Ang induced vasopressin release. For this purpose, double in situ hybridization was performed using a radioactive AT1A receptor riboprobe and a digoxygenin labeled AVP oligoprobe, and immunohistochemical localization of the glial marker glial fibrillary acidic protein (GFAP) on the same brain slice. The results show neuronal expression of AT1A receptor mRNA mainly in dorsal and medial parvocellular parts of the PVN, its localization in some magnocellular PVN neurons and the absence of its expression in AVP producing neurons either in the PVN or in the SON. Thus, while indirect evidence indicates the involvement of the AT1A receptor subtype in the regulation of CRH and oxytocin release, the stimulation of vasopressinergic neurons is likely due to indirect mechanisms, or to a yet unknown type of angiotensin receptor.
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PMID:Comparative expression of vasopressin and angiotensin type-1 receptor mRNA in rat hypothalamic nuclei: a double in situ hybridization study. 875 Aug 69

Angiotensin receptors have recently become a focus of scientific interest due to the recent development of specific receptor ligands which allow to distinguish between various angiotensin II receptor subtypes, notably the angiotensin II type 1 receptor (AT1) and angiotensin II type 2 receptor (AT2). Although both receptors belong to the seven transmembrane domain receptor family they feature less than 35% homology and differ in their signal transduction mechanisms and in the effects mediated. In the brain, both angiotensin receptor types and probably some further subtypes are present and have been localized in distinct regions. In the adult brain, the AT1 receptor dominates by far and is responsible for most of the known central actions of angiotensin peptides, for example blood pressure increase, release of vasopressin from the pituitary gland, natriuresis, drinking and induction of immediate early genes in distinct brain areas. Some of the AT1 receptor-mediated effects have been shown to be enhanced by blockade of AT2 receptors in the brain suggesting that the central AT2 receptor can exert an inhibitory control on AT1 receptor-mediated actions in the brain.
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PMID:Angiotensin receptors in the brain. 877 41

Normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) received aminopeptidase M (AmM) delivered into the paraventricular nucleus of the hypothalamus (PVN). Resulting changes in blood pressure were recorded in both anesthetized and alert animals. The findings indicate significant dose-determined decreases in blood pressure in members of both strains with SHR more responsive than WKY rats. The respective drops in blood pressure for members within each strain were equivalent for the anesthetized and alert conditions. Pretreatment with the specific angiotensin receptor antagonist, sarthran, [Sar1, Thr2] Angll, into the PVN greatly diminished these responses, suggesting the involvement of the brain angiotensin system. Additionally, a sympathetic nervous system blocker, hexamethonium, and the arginine vasopressin antagonist, Pmp1, O-Me-Tyr2-[Arg] vasopressin, were peripherally administered to assess the potential contributions of these systems to cardiovascular regulation by the brain angiotensin system. The use of these blockers, individually and combined, attenuated responsiveness to infusion of AmM into the PVN. We conclude that AmM can act as a hypotensive agent in both SHR and WKY rats, and that this decrease in blood pressure is at least partially mediated via the brain angiotensin system although other systems may play a role.
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PMID:Microinfusion of aminopeptidase M into the paraventricular nucleus of the hypothalamus in normotensive and hypertensive rats. 896 89

The explosion of new knowledge about the complex mechanisms mediating high blood pressure is providing new targets for drug therapy of hypertension and other cardiovascular disorders. This article reviews the current status of several new approaches in the management of hypertension, including vasopressin antagonists, natriuretic peptide clearance inhibitors, endothelin antagonists, renin inhibitors, angiotensin receptor antagonists, and selective T-type calcium ion channel antagonists.
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PMID:New developments in drug therapy of hypertension. 935 4

The involvement of central angiotensinergic and cholinergic mechanisms in the effects of the intracerebroventricularly injected somatostatin analog octreotide (Oct) on drinking, blood pressure, and vasopressin secretion in the rat was investigated. Intracerebroventricular Oct elicited prompt drinking lasting for 10 min. Water consumption depended on the dose of Oct (0.01, 0.1, and 0. 4 microgram). The drinking response to Oct was inhibited by pretreatments with the intracerebroventricularly injected angiotensin-converting enzyme inhibitor captopril, the AT(1)/AT(2) angiotensin receptor antagonist saralasin, the selective AT(1) receptor antagonist losartan, or the muscarinic cholinergic receptor antagonist atropine. The dipsogenic effect of Oct was not altered by prior subcutaneous injection of naloxone. Oct stimulated vasopressin secretion and enhanced blood pressure. These responses were also blocked by pretreatments with captopril or atropine. Previous reports indicate that the central angiotensinergic and cholinergic mechanisms stimulate drinking and vasopressin secretion independently. We suggest that somatostatin acting on sst2 or sst5 receptors modulates central angiotensinergic and cholinergic mechanisms involved in the regulation of fluid balance.
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PMID:Octreotide-induced drinking, vasopressin, and pressure responses: role of central angiotensin and ACh. 1089 91


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