Differential regulation of atrial contraction by P1 and P2 purinoceptors in normotensive and spontaneously hypertensive rats

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dc.contributor.authorDantas Rodrigues, Juliano Quintella [UNIFESP]
dc.contributor.authorSilva, Edilson Dantas da [UNIFESP]
dc.contributor.authorGalvao, Kleber de Magalhaes [UNIFESP]
dc.contributor.authorMiranda-Ferreira, Regiane [UNIFESP]
dc.contributor.authorCaricati-Neto, Afonso [UNIFESP]
dc.contributor.authorJurkiewicz, Neide Hyppolito [UNIFESP]
dc.contributor.authorGarcia, Antonio G.
dc.contributor.authorJurkiewicz, Aron [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniv Autonoma Madrid
dc.date.accessioned2016-01-24T14:35:23Z
dc.date.available2016-01-24T14:35:23Z
dc.date.issued2014-03-01
dc.description.abstractIn the normotensive rat atrium, adenosine-5'-triphosphate and uridine-5'-triphosphate exert a biphasic effect consisting of an initial negative inotropic effect (NIE) followed by a subsequent positive inotropic effect (PIE). We comparatively studied these responses in normotensive Wistar rats (NWRs) and spontaneously hypertensive rats (SHRs). Compared with NWRs, the NIE responses in the atria were lower and the PIE responses were higher in SHRs. the P1 purinoceptor antagonist, D 8-cyclopentyl-1,3- dipropylxanthine, partially blocked the NIE responses of both ATP and UTP and mildly enhanced the PIE responses in both NWRs and SHRs. Furthermore, the P2 purinoceptor blockers suramin and pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid tetrasodium salt induced a pronounced block of the PIE responses in both atria types. the PIE responses to ATP were inhibited more efficiently by nifedipine. These responses were depressed by ryanodine and, to a lesser extent, carbonyl cyanide 3-chlorophenylhydrazone in SHR atria compared with NWR atria. the higher responses in SHR rats suggest the existence of an augmented endoplasmic reticulum Ca2+ store and faster mitochondrial Ca2+ cycling in SHR atria compared with NWR atria. These data support the hypothesis that a dysfunction of purinergic neurotransmission and enhanced sympathetic activity are contributing factors in the pathogenesis of hypertension.en
dc.description.affiliationFed Univ São Paulo UNIFESP, Dept Pharmacol, BR-04044020 São Paulo, Brazil
dc.description.affiliationUniv Autonoma Madrid, Inst Teofilo Hernando, Madrid, Spain
dc.description.affiliationUnifespFed Univ São Paulo UNIFESP, Dept Pharmacol, BR-04044020 São Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent210-219
dc.identifierhttp://dx.doi.org/10.1038/hr.2013.146
dc.identifier.citationHypertension Research. London: Nature Publishing Group, v. 37, n. 3, p. 210-219, 2014.
dc.identifier.doi10.1038/hr.2013.146
dc.identifier.issn0916-9636
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/37505
dc.identifier.wosWOS:000332451200004
dc.language.isoeng
dc.publisherNature Publishing Group
dc.relation.ispartofHypertension Research
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjecthypertensionen
dc.subjectisolated left atriumen
dc.subjectP1 and P2 purinergic receptorsen
dc.subjectSHRen
dc.titleDifferential regulation of atrial contraction by P1 and P2 purinoceptors in normotensive and spontaneously hypertensive ratsen
dc.typeinfo:eu-repo/semantics/article
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