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dc.contributor.authorCrestani, Carlos Cesar [UNESP]
dc.contributor.authorSilva, Andreia Lopes da
dc.contributor.authorScopinho, America A.
dc.contributor.authorRuginsk, Silvia G.
dc.contributor.authorUchoa, Ernane T.
dc.contributor.authorCorrea, Fernando M. A.
dc.contributor.authorElias, Lucila L. K.
dc.contributor.authorAntunes-Rodrigues, Jose
dc.contributor.authorResstel, Leonardo B. M.
dc.date.accessioned2015-03-18T15:54:04Z
dc.date.available2015-03-18T15:54:04Z
dc.date.issued2014-10-15
dc.identifierhttp://dx.doi.org/10.1016/j.taap.2014.08.012
dc.identifier.citationToxicology And Applied Pharmacology. San Diego: Academic Press Inc Elsevier Science, v. 280, n. 2, p. 245-255, 2014.
dc.identifier.issn0041-008X
dc.identifier.urihttp://hdl.handle.net/11449/116754
dc.description.abstractThe aim of the present work was to establish a time-course correlation between vascular and autonomic changes that contribute to the development of hypertension during ethanol ingestion in rats. For this, male Wistar rats were subjected to the intake of increasing ethanol concentrations in their drinking water during four weeks. Ethanol effects were investigated at the end of each week. Mild hypertension was already observed at the first week of treatment, and a progressive blood pressure increase was observed along the evaluation period. Increased pressor response to phenylephrine was observed from first to fourth week. alpha(1)-adrenoceptor protein in the mesenteric bed was enhanced at the first week, whereas beta(2)-adrenoceptor protein in the aorta was reduced after the second week. In the third week, ethanol intake facilitated the depressor response to sodium nitroprusside, whereas in the fourth week it reduced nitrate content in aorta and increased it plasma. The bradycardic component of the baroreflex was impaired, whereas baroreflex tachycardia was enhanced at the third and fourth weeks. AT(1A) receptor and C-type natriuretic peptide (CNP) mRNAs in the nucleus tractus solitarius were increased at the fourth week. These findings suggest that increased vascular responsiveness to vasoconstrictor agents is possibly a link factor in the development and maintenance of the progressive hypertension induced by ethanol consumption. Additionally, baroreflex changes are possibly mediated by alterations in angiotensinergic mechanisms and CNP content within the brainstem, which contribute to maintaining the hypertensive state in later phases of ethanol ingestion. Facilitated vascular responsiveness to nitric oxide seems to counteract ethanol-induced hypertension. (C) 2014 Elsevier Inc. All rights reserved.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipNational Council for Scientific and Technological Development
dc.format.extent245-255
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofToxicology And Applied Pharmacology
dc.sourceWeb of Science
dc.subjectBaroreflexen
dc.subjectVascular reactivityen
dc.subjectAdrenoceptoren
dc.subjectNitric oxideen
dc.subjectNitrateen
dc.subjectNucleus tractus solitariusen
dc.titleCardiovascular alterations at different stages of hypertension development during ethanol consumption: Time-course of vascular and autonomic changesen
dc.typeArtigo
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderElsevier B.V.
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.description.affiliationUniv Estadual Paulista, Sch Pharmaceut Sci, Dept Nat Act Principles & Toxicol, Sao Paulo, Brazil
dc.description.affiliationUniv Sao Paulo, Sch Med Ribeirao Preto, Dept Physiol, BR-14049900 Ribeirao Preto, SP, Brazil
dc.description.affiliationUniv Sao Paulo, Sch Med Ribeirao Preto, Dept Pharmacol, BR-14049900 Ribeirao Preto, SP, Brazil
dc.description.affiliationUnespUniv Estadual Paulista, Sch Pharmaceut Sci, Dept Nat Act Principles & Toxicol, Sao Paulo, Brazil
dc.identifier.doi10.1016/j.taap.2014.08.012
dc.identifier.wosWOS:000344444700006
dc.rights.accessRightsAcesso restrito
dc.description.sponsorshipIdFAPESP: 09/51676-9
dc.description.sponsorshipIdFAPESP: 08/50611-8
dc.description.sponsorshipIdNational Council for Scientific and Technological Development301827/2011/7
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Ciências Farmacêuticas, Araraquarapt
dc.identifier.lattes1117432571971568
unesp.author.lattes1117432571971568
unesp.author.orcid0000-0002-1942-858X[1]
dc.relation.ispartofjcr3.616
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