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dc.contributor.authorPriviero, Fernanda B. M.
dc.contributor.authorTeixeira, Cleber E.
dc.contributor.authorClaudino, Mario A.
dc.contributor.authorDe Nucci, Gilberto
dc.contributor.authorZanesco, Angelina
dc.contributor.authorAntunes, Edson
dc.date.accessioned2014-05-20T15:23:20Z
dc.date.available2014-05-20T15:23:20Z
dc.date.issued2007-10-01
dc.identifierhttp://dx.doi.org/10.1016/j.ejphar.2007.05.060
dc.identifier.citationEuropean Journal of Pharmacology. Amsterdam: Elsevier B.V., v. 571, n. 2-3, p. 189-196, 2007.
dc.identifier.issn0014-2999
dc.identifier.urihttp://hdl.handle.net/11449/34143
dc.description.abstractLong-term propranolol treatment reduces arterial blood pressure in hypertensive individuals mainly by reducing peripheral vascular resistance, but mechanisms underlying their vasodilatory effect remain poorly investigated. This study aimed to investigate whether long-term propranolol administration ameliorates the impairment of relaxing responses of aorta and mesenteric artery from rats made hypertensive by chronic nitric oxide (NO) deficiency, and underlying mechanisms mediating this phenomenon. Male Wistar rats were treated with N-omega-Nitro-L-arginine methyl ester (L-NAME; 20 mg/rat/day) for four weeks. DL-Propranolol (30 mg/rat/day) was given concomitantly to L-NAME in the drinking water. Treatment with L-NAME markedly increased blood pressure, an effect largely attenuated by DL-propranolol. In phenylephrine-precontracted aortic rings, the reduction of relaxing responses for acetylcholine (0.001-10 mu M) in L-NAME group was not modified by DL-propranolol, whereas in mesenteric rings the impairment of acetylcholine-induced relaxation by L-NAME was significantly attenuated by DL-propranolol. In mesenteric rings precontracted with KCl (80 MM), DL-propranolol failed to attenuate the impairment of acetylcholine-induced relaxation by L-NAME. The contractile responses to extracellular CaCl2 (1-10 mM) were increased in L-NAME group, and co-treatment with DL-propranolol reduced this response in both preparations in most Ca2+ concentrations used. The NO2/NO3 plasma levels and superoxide dismutase (SOD) activity were reduced in L-NAME-treated rats, both of which were significantly prevented by DL-propranolol. In conclusion, propranolol-induced amplification of the relaxation to acetylcholine in mesenteric arteries from L-NAME-treated rats is sensitive to depolarization. Additional mechanisms involving blockade of Ca2+ entry in the vascular smooth muscle and increase in NO bioavailability contributes to beneficial effects of long-term propranolol treatment. (C) 2007 Elsevier B.V. All rights reserved.en
dc.format.extent189-196
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofEuropean Journal of Pharmacology
dc.sourceWeb of Science
dc.subjectendothelium-derived hyperpolarizing factorpt
dc.subjectendothelial dysfunctionpt
dc.subjectbeta-adrenoceptor antagonistpt
dc.subjectnitric oxide bioavailabilitypt
dc.subjectarterial reactivitypt
dc.titleVascular effects of long-term propranolol administration after chronic nitric oxide blockadeen
dc.typeArtigo
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderElsevier B.V.
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.description.affiliationUniv Estadual Campinas, Fac Med Sci, Dept Pharmacol, BR-13084971 Campinas, SP, Brazil
dc.description.affiliationUniv São Paulo State, UNESP, Dept Educ Phys, São Paulo, Brazil
dc.description.affiliationUnespUniv São Paulo State, UNESP, Dept Educ Phys, São Paulo, Brazil
dc.identifier.doi10.1016/j.ejphar.2007.05.060
dc.identifier.wosWOS:000250043400015
dc.rights.accessRightsAcesso restrito
unesp.campusUniversidade Estadual Paulista (UNESP), Instituto de Biociências, Rio Claropt
dc.identifier.lattes4472007237545596
unesp.author.lattes4472007237545596
unesp.author.orcid0000-0002-3590-9607[3]
unesp.author.orcid0000-0002-4346-7941[4]
unesp.author.orcid0000-0003-2201-8247[6]
unesp.author.orcid0000-0002-6022-2081[1]
dc.relation.ispartofjcr3.040
dc.relation.ispartofsjr1,057
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