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dc.contributor.authorClaudino, Mario A.
dc.contributor.authorFranco-Penteado, Carla F.
dc.contributor.authorPriviero, Fernanda B. M.
dc.contributor.authorCamargo, Enilton A.
dc.contributor.authorTeixeira, Simone A.
dc.contributor.authorMuscara, Marcelo N.
dc.contributor.authorDe Nucci, Gilberto
dc.contributor.authorZanesco, Angelina
dc.contributor.authorAntunes, Edson
dc.date.accessioned2014-05-20T15:33:19Z
dc.date.available2014-05-20T15:33:19Z
dc.date.issued2010-04-01
dc.identifierhttp://dx.doi.org/10.1016/j.urology.2009.05.098
dc.identifier.citationUrology. New York: Elsevier B.V., v. 75, n. 4, p. 961-967, 2010.
dc.identifier.issn0090-4295
dc.identifier.urihttp://hdl.handle.net/11449/41978
dc.description.abstractOBJECTIVES To test the hypothesis that glyco protein 91phox (gp91(phox)) subunit of nicotinamide adenine dinucleotide phosphate [NAD(P) H] oxidase is a fundamental target for physical activity to ameliorate erectile dysfunction (ED). Vascular risk factors are reported to contribute to ED. Regular physical exercise prevents cardiovascular diseases by increasing nitric oxide (NO) production and/or decreasing NO inactivation.METHODS Male Wistar rats received the NO synthesis inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) for 4 weeks, after which animals were submitted to a run training program for another 4 weeks. Erectile functions were evaluated by in vitro cavernosal relaxations and intracavernous pressure measurements. Expressions of gp91(phox) subunit and neuronal nitric oxidase synthase in erectile tissue, as well as superoxide dismutase activity and nitrite/nitrate (NO(x)) levels were determined.RESULTS The in vitro acetylcholine-and electrical field stimulation-induced cavernosal relaxations, as well as the increases in intracavernous pressure were markedly reduced in sedentary rats treated with L-NAME. Run training significantly restored the impaired cavernosal relaxations. No alterations in the neuronal nitric oxidase synthase protein expression (and its variant penile neuronal nitric oxidase synthase) were detected. A reduction of NO(x) levels and superoxide dismutase activity was observed in L-NAME-treated animals, which was significantly reversed by physical training. Gene expression of subunit gp91(phox) was enhanced by approximately 2-fold in erectile tissue of L-NAME-treated rats, and that was restored to basal levels by run training.CONCLUSIONS Our study shows that ED seen after long-term L-NAME treatment is associated with gp91(phox) subunit upregulation and decreased NO bioavailability. Exercise training reverses the increased oxidative stress in NO-deficient rats, ameliorating the ED. UROLOGY 75: 961-967, 2010. (C) 2009 Elsevier B.V.en
dc.format.extent961-967
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofUrology
dc.sourceWeb of Science
dc.titleUpregulation of gp91(phox) Subunit of NAD(P)H Oxidase Contributes to Erectile Dysfunction Caused by Long-term Nitric Oxide Inhibition in Rats: Reversion by Regular Physical Trainingen
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.contributor.institutionUniversidade de São Paulo (USP)
dc.description.affiliationUniv Estadual Campinas, Dept Pharmacol, Fac Med Sci, Hematol & Hemotherapy Ctr, BR-13084971 São Paulo, Brazil
dc.description.affiliationState Univ São Paulo UNESP, Inst Biosci, Dept Phys Educ, São Paulo, Brazil
dc.description.affiliationUniv São Paulo, Dept Pharmacol, Inst Biomed Sci, BR-09500900 São Paulo, Brazil
dc.description.affiliationUnespState Univ São Paulo UNESP, Inst Biosci, Dept Phys Educ, São Paulo, Brazil
dc.identifier.doi10.1016/j.urology.2009.05.098
dc.identifier.wosWOS:000276258300037
dc.rights.accessRightsAcesso restrito
unesp.campusUniversidade Estadual Paulista (Unesp), Instituto de Biociências, Rio Claropt
dc.identifier.lattes4472007237545596
unesp.author.lattes4472007237545596
unesp.author.orcid0000-0002-8515-5030[5]
unesp.author.orcid0000-0002-4346-7941[7]
unesp.author.orcid0000-0002-3590-9607[1]
unesp.author.orcid0000-0003-2201-8247[9]
unesp.author.orcid0000-0002-8342-5586[6]
unesp.author.orcid0000-0002-6022-2081[3]
dc.relation.ispartofjcr2.300
dc.relation.ispartofsjr1,111
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