Impaired function of alpha-2 adrenoceptors in smooth muscle of mesenteric arteries from spontaneously hypertensive rats

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dc.contributor.authorFeres, Teresa [UNIFESP]
dc.contributor.authorBorges, Antonio Carlos Romao [UNIFESP]
dc.contributor.authorSilva, Eneida de Gusmão [UNIFESP]
dc.contributor.authorPaiva, Antonio Cechelli de Mattos [UNIFESP]
dc.contributor.authorPaiva, Therezinha Bandiera [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T12:30:41Z
dc.date.available2016-01-24T12:30:41Z
dc.date.issued1998-11-01
dc.description.abstract1 the alpha(2)-adrenoceptor function in mesenteric arteries of spontaneously hypertensive rats (SHR) was investigated by comparing membrane potential changes in response to adrenergic agonists in preparations from female SHR, Wistar-Kyoto (WKY) and normotensive Wistar rats (NWR).2 Resting membrane potential was found to be less negative in mesenteric arteries from SHR than in those from NWR and WKY. Apamin induced a decrease in the membrane potential of mesenteric artery rings without endothelium from NWR and WKY, but had no effects in those from SHR. Both UK 14,304 and adrenaline, in the presence of prazosin, induced a hyperpolarization that was significantly lower in de-endothelialized mesenteric rings from SHR than in those from NWR and WKY. in mesenteric rings with endothelium, however, similar hyperpolarization was observed in the three strains.3 in NWR mesenteric rings with endothelium the hyperpolarization induced by activation of alpha(2)-adrenoceptors was abolished by apamin, whereas in intact SHR mesenteric rings this hyperpolarization was slightly reduced by apamin and more efficiently reduced by N-omega-nitro-L-arginine.4 It is concluded that the activity of potassium channels coupled to alpha(2)-adrenoceptors is altered in the smooth muscle cells of SHR mesenteric arteries, contributing to their less negative membrane potential. On the other hand, the endothelial alpha(2)-receptors are functioning in mesenteric vessels from SHR and their stimulation induces a hyperpolarization mainly through the release of nitric oxide.en
dc.description.affiliationEscola Paulista Med, Dept Biophys, BR-04023062 São Paulo, Brazil
dc.description.affiliationUnifespEscola Paulista Med, Dept Biophys, BR-04023062 São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extent1144-1149
dc.identifierhttp://dx.doi.org/10.1038/sj.bjp.0702177
dc.identifier.citationBritish Journal of Pharmacology. Basingstoke: Stockton Press, v. 125, n. 6, p. 1144-1149, 1998.
dc.identifier.doi10.1038/sj.bjp.0702177
dc.identifier.issn0007-1188
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/25970
dc.identifier.wosWOS:000077085800005
dc.language.isoeng
dc.publisherStockton Press
dc.relation.ispartofBritish Journal of Pharmacology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectalpha-2 adrenoceptorsen
dc.subjectmesenteric arteriesen
dc.subjectendotheliumen
dc.subjectspontaneously hypertensive ratsen
dc.subjectpotassium channelsen
dc.subjectmembrane potentialen
dc.titleImpaired function of alpha-2 adrenoceptors in smooth muscle of mesenteric arteries from spontaneously hypertensive ratsen
dc.typeinfo:eu-repo/semantics/article
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