Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/33897
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dc.contributor.authorLoiola, Rodrigo Azevedo [UNIFESP]
dc.contributor.authorReis, Felipe Castellani Gomes dos [UNIFESP]
dc.contributor.authorMári-Kawamoto, Elisa [UNIFESP]
dc.contributor.authorScavone, Cristoforo [UNIFESP]
dc.contributor.authorAbdalla, Dulcineia Saes Parra [UNIFESP]
dc.contributor.authorFernandes, Liliam [UNIFESP]
dc.contributor.authorPesquero, João Bosco [UNIFESP]
dc.date.accessioned2016-01-24T14:17:01Z-
dc.date.available2016-01-24T14:17:01Z-
dc.date.issued2011-08-01
dc.identifierhttp://dx.doi.org/10.1016/j.peptides.2011.06.010
dc.identifier.citationPeptides. New York: Elsevier B.V., v. 32, n. 8, p. 1700-1705, 2011.
dc.identifier.issn0196-9781
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/33897-
dc.description.abstractKinin B-1 and B-2 receptors play an essential role in inflammatory process and cardiovascular homeostasis. the present study investigated the vascular reactivity and nitric oxide (NO) generation in the isolated mesenteric arteriolar bed from B-1 (B-1(-/-)) and B-2 receptor (B-2(-/-)) knockout mice. Endothelial-dependent relaxation was significantly decreased in arterioles from both B-1(-/-) and B-2(-/-) in comparison to wild type (WT) mice, with no differences for endothelial-independent relaxating or vasoconstrictor agents. Plasmatic and vascular NO production were markedly reduced in both B-1(-/-) and B-2(-/-). in contrast, in the presence of L-arginine, Ca2+ and co-factors for the enzyme, NO synthase activity was higher in homogenates of mesenteric vessels of B-1(-/-) and B-2(-/-). the present study demonstrated that targeted deletion of B-1 or B-2 receptor gene in mice induces important alterations in the vascular reactivity of resistance vessels and NO metabolism. the severe impairment in the endothelial-mediated vasodilation accompanied by decreased NO bioavailability, despite the augmented NOS activity, strongly indicates an exacerbation of NO inactivation in B-1(-/-) and B-2(-/-) vessels. the present data provide valuable information in order to clarify the relevance of kinin receptors in regulating vascular physiology and may point to new approaches regarding its correlation with endothelial dysfunction, oxidative stress and NO availability. (C) 2011 Elsevier Inc. All rights reserved.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.format.extent1700-1705
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofPeptides
dc.rightsAcesso aberto
dc.subjectB-1 receptoren
dc.subjectB-2 receptoren
dc.subjectKnockouten
dc.subjectBradykininen
dc.subjectVascular reactivityen
dc.subjectNitric oxideen
dc.titleRole of vascular Kinin B-1 and B-2 receptors in endothelial nitric oxide metabolismen
dc.typeArtigo
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.description.affiliationUniversidade Federal de São Paulo, Dept Biol Sci, BR-09972270 Diadema, SP, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Biophys, São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Pharmacol, São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Clin Anal & Toxicol, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Biol Sci, BR-09972270 Diadema, SP, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Biophys, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Pharmacol, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Clin Anal & Toxicol, São Paulo, Brazil
dc.description.sponsorshipIDFAPESP: 2007/59039-2
dc.description.sponsorshipIDFAPESP: 2008/06676-8
dc.identifier.fileWOS000294572800018.pdf
dc.identifier.doi10.1016/j.peptides.2011.06.010
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000294572800018
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