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Use este identificador para citar ou linkar para este item: https://repositorio.ufba.br/handle/ri/16390
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dc.contributor.authorVeras, Robson Cavalcante-
dc.contributor.authorRodrigues, Karoline Gomes-
dc.contributor.authorFernandes, Maria do Carmo de Alustau-
dc.contributor.authorGonçalves, Islania Giselia Albuquerque-
dc.contributor.authorBarros, André Luis Branco de-
dc.contributor.authorAlves, Ricardo José-
dc.contributor.authorNakao, Lia Sumie-
dc.contributor.authorBraga, Valdir de Andrade-
dc.contributor.authorVasconcelos, Darizy Flavia Silva Amorim de-
dc.contributor.authorMedeiros, Isac Almeida de-
dc.creatorVeras, Robson Cavalcante-
dc.creatorRodrigues, Karoline Gomes-
dc.creatorFernandes, Maria do Carmo de Alustau-
dc.creatorGonçalves, Islania Giselia Albuquerque-
dc.creatorBarros, André Luis Branco de-
dc.creatorAlves, Ricardo José-
dc.creatorNakao, Lia Sumie-
dc.creatorBraga, Valdir de Andrade-
dc.creatorVasconcelos, Darizy Flavia Silva Amorim de-
dc.creatorMedeiros, Isac Almeida de-
dc.date.accessioned2014-10-10T15:13:34Z-
dc.date.issued2013-
dc.identifier.issn0160-2446-
dc.identifier.urihttp://repositorio.ufba.br/ri/handle/ri/16390-
dc.descriptionTexto completo: acesso restrito. p. 58–66pt_BR
dc.description.abstractFor many years, nitric oxide (NO) has been studied as an important mediator in the control of vascular tone. Endothelial deficiencies that diminish NO production can result in the development of several future cardiovascular diseases, such as hypertension and arteriosclerosis. In this context, new drugs with potential ability to donate NO have been studied. In this study, 3 aromatic oximes [benzophenone oxime, 4-Cl-benzophenone oxime, and E-cinnamaldehyde oxime (E-CAOx)] induced vasorelaxation in endothelium-denuded and intact superior mesenteric rings precontracted with phenylephrine. E-CAOx demonstrated the most potent effect, and its mechanism of action was evaluated. Vascular reactivity experiments demonstrated that the effect of E-CAOx was reduced by the presence of 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide, 1H[1,2,4,]oxadiazolo[4,3-a]quinoxalin-1-one, and (Rp)-8-(para-chlorophenylthio)guanosine-3',5'-cyclic monophosphorothioate, suggesting the participation of NO/sGC/PKG pathway. NO donation seems to be mediated through nicatinamide adenine dinucleotide phosphate-dependent reductases because 7-ethoxyresorufin decreased the effect of E-CAOx on vascular reactivity and reduced NO formation as detected by flow cytometry using the NO indicator diaminofluorescein 4,5-diacetate. Further downstream of NO donation, K+ subtype channels were also shown to be involved in the E-CAOx vasorelaxant effect. The present study showed that E-CAOx acts like an NO donor, activating NO/sGC/PKG pathway and thus K+ channels.pt_BR
dc.language.isoenpt_BR
dc.rightsAcesso Abertopt_BR
dc.sourcehttp://dx.doi.org/10.1097/FJC.0b013e31829013ffpt_BR
dc.subjectEndotheliumpt_BR
dc.subjectNO donorpt_BR
dc.subjectOximept_BR
dc.subjectRatpt_BR
dc.subjectVasorelaxationpt_BR
dc.titleParticipation of nitric oxide pathway in the relaxation response induced by E-cinnamaldehyde oxime in superior mesenteric artery isolated from ratspt_BR
dc.title.alternativeJournal of Cardiovascular Pharmacologypt_BR
dc.typeArtigo de Periódicopt_BR
dc.identifier.numberv. 62, n. 1pt_BR
dc.embargo.liftdate10000-01-01-
Aparece nas coleções:Artigo Publicado em Periódico (FAR)

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