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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampCalmasini, Fabiano Beraldipt_BR
dc.contributor.authorunicampSilveira, Leiria Luiz Osoriopt_BR
dc.contributor.authorunicampAlves Junior, Marcos Josépt_BR
dc.contributor.authorunicampAlexandre, Eduardo Costapt_BR
dc.contributor.authorunicampMónica, Fabíola Zakia Tauficpt_BR
dc.contributor.authorunicampAntunes, Edsonpt_BR
dc.typeArtigopt_BR
dc.titleIncreased Rho-kinase-mediated prostate contractions associated with impairment of Beta-adrenergic-camp-signaling pathway by chronic nitric oxide deficiencypt_BR
dc.contributor.authorCalmasini, Fabiano Beraldipt_BR
dc.contributor.authorSilveira, Leiria Luiz Osorio| Alves Junior,Marcos Josept_BR
dc.contributor.authorBau, Fernando Ricardopt_BR
dc.contributor.authorAlexandre, Eduardo Costapt_BR
dc.contributor.authorSilva,Fabio Henriquept_BR
dc.contributor.authorMonica, Fabiola Zakiapt_BR
dc.contributor.authorAntunes, Edsonpt_BR
unicamp.author.emailedson.antunes@uol.com.brpt_BR
unicamp.authorAntunes, Edson] Univ Estadual Campinas, UNICAMP, Fac Med Sci, Dept Pharmacol, BR-13084971 Campinas, SP, Brazilpt_BR
unicamp.author.external[Calmasini, Fabiano Beraldipt
unicamp.author.externalSilveira Leiria, Luiz Osoriopt
unicamp.author.externalAlves Junior, Marcos Josept
unicamp.author.externalBau, Fernando Ricardopt
unicamp.author.externalAlexandre, Eduardo Costapt
unicamp.author.externalSilva, Fabio Henriquept
unicamp.author.externalMonica, Fabiola Zakiapt
dc.subjectPróstatapt_BR
dc.subjectÓxido nítricopt_BR
dc.subjectQuinases associadas a Rhopt_BR
dc.subjectNG-nitroarginina metil ésterpt_BR
dc.subject.otherlanguageProstatept_BR
dc.subject.otherlanguageNitric oxidept_BR
dc.subject.otherlanguageRho-associated kinasespt_BR
dc.subject.otherlanguageNG-nitroarginine methyl esterpt_BR
dc.description.abstractImpairment of nitric oxide (NO) - cyclic GMP signaling pathway is likely to contribute to human begnin prostate hyperplasia (BPH). In the present study we have used a model of chronic NO synthesis inhibition to evaluate the functional alterations of prostate smooth muscle (PSM) machinery, and involvement of Rho-kinase pathway. Wistar rats were treated with the NO inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME, 20 mg/kg/day; 4 weeks), after which contractile responses to phenylephrine (alpha(1)-adrenoceptor agonist; 1 nM to 100 mu M), carbachol (muscarinic agonist; 1 nM to 1 mM) and alpha,beta-methylene ATP (P2X receptor agonist; 1-10 mu M), as well as to electrical-field stimulation (EFS; 1-32 Hz) were evaluated. PSM relaxations to isoproterenol (non-selective beta-adrenoceptor agonist, 0.1 nM to 10 mu M) and sodium nitroprusside (NO donor, 1 nM to 10 mM) were also evaluated. The ratio prostate weight/body weight was 22% greater (P< 0.05) in L-NAME compared with control group. The PSM contractions to phenylephrine, carbachol and alpha,beta-methylene ATP were higher in L-NAME (E-max: 3.85 +/- 0.25, 3.52 +/- 0.35 and 2.03 +/- 0.2 mN, respectively) compared with control group (E-max: 3.08 +/- 0.17, 2.37 +/- 0.18 and 1.57 +/- 0.18 mN, respectively). The PSM contractions induced by EFS were also significantly greater in L-NAME group. Prior incubation with the Rho-kinase inhibitor Y27632 (1 mu M) fully reversed the enhanced contractions to phenylephrine and carbachol. Isoproterenol-induced PSM relaxations were 34% lower in L-NAME group, which was associated with reduced levels of cAMP in prostate tissue. The relaxations to sodium nitroprusside remained unaltered in L-NAME group. In summary, chronic NO deficiency leads to increased Rho-kinase-mediated PSM contractile responses accompanied by impairment of beta-adrenergic-cAMP-signaling pathway. (C) 2015 Elsevier B.V. All rights reserved.en
dc.description.abstractImpairment of nitric oxide (NO) - cyclic GMP signaling pathway is likely to contribute to human begnin prostate hyperplasia (BPH). In the present study we have used a model of chronic NO synthesis inhibition to evaluate the functional alterations of prostate smooth muscle (PSM) machinery, and involvement of Rho-kinase pathway. Wistar rats were treated with the NO inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME, 20 mg/kg/day; 4 weeks), after which contractile responses to phenylephrine (alpha(1)-adrenoceptor agonist; 1 nM to 100 mu M), carbachol (muscarinic agonist; 1 nM to 1 mM) and alpha,beta-methylene ATP (P2X receptor agonist; 1-10 mu M), as well as to electrical-field stimulation (EFS; 1-32 Hz) were evaluated. PSM relaxations to isoproterenol (non-selective beta-adrenoceptor agonist, 0.1 nM to 10 mu M) and sodium nitroprusside (NO donor, 1 nM to 10 mM) were also evaluated. The ratio prostate weight/body weight was 22% greater (P< 0.05) in L-NAME compared with control group. The PSM contractions to phenylephrine, carbachol and alpha,beta-methylene ATP were higher in L-NAME (E-max: 3.85 +/- 0.25, 3.52 +/- 0.35 and 2.03 +/- 0.2 mN, respectively) compared with control group (E-max: 3.08 +/- 0.17, 2.37 +/- 0.18 and 1.57 +/- 0.18 mN, respectively). The PSM contractions induced by EFS were also significantly greater in L-NAME group. Prior incubation with the Rho-kinase inhibitor Y27632 (1 mu M) fully reversed the enhanced contractions to phenylephrine and carbachol. Isoproterenol-induced PSM relaxations were 34% lower in L-NAME group, which was associated with reduced levels of cAMP in prostate tissue. The relaxations to sodium nitroprusside remained unaltered in L-NAME group. In summary, chronic NO deficiency leads to increased Rho-kinase-mediated PSM contractile responses accompanied by impairment of beta-adrenergic-cAMP-signaling pathwaypt
dc.relation.ispartofEuropean Journal of Pharmacologypt_BR
dc.relation.ispartofabbreviationEur. J. Pharmacol.pt_BR
dc.publisher.cityAmsterdãpt_BR
dc.publisher.countryHolandapt_BR
dc.publisherElsevierpt_BR
dc.date.issued2015pt_BR
dc.date.monthofcirculationJulypt_BR
dc.identifier.citationIncreased Rho-kinase-mediated Prostate Contractions Associated With Impairment Of Beta-adrenergic-camp-signaling Pathway By Chronic Nitric Oxide Deficiency. Elsevier Science Bv, v. 758, p. 24-30 Jul-2015.pt_BR
dc.language.isoengpt_BR
dc.description.volume758pt_BR
dc.description.firstpage24pt_BR
dc.description.lastpage30pt_BR
dc.rightsfechadopt_BR
dc.sourceWOSpt_BR
dc.sourceWOSpt_br
dc.identifier.issn0014-2999pt_BR
dc.identifier.wosidWOS:000353787300004pt_BR
dc.identifier.doi10.1016/j.ejphar.2015.03.057pt_BR
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0014299915002861pt_BR
dc.description.sponsorshipFAPESP – FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOpt_BR
dc.description.sponsorshipCAPES – COORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL E NÍVEL SUPERIORpt_BR
dc.description.sponsorship1FAPESP – FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOpt_BR
dc.description.sponsorship1CAPES – COORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL E NÍVEL SUPERIORpt_BR
dc.description.sponsordocumentnumberCAPES [01P-03887/2011]pt
dc.date.available2016-06-07T13:35:11Z-
dc.date.accessioned2016-06-07T13:35:11Z-
dc.description.provenanceMade available in DSpace on 2016-06-07T13:35:11Z (GMT). No. of bitstreams: 1 wos_000353787300004.pdf: 408872 bytes, checksum: 7e55c555181c3019a9892dbb4334e195 (MD5) Previous issue date: 2015en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/244072-
dc.contributor.departmentDepartamento de Farmacologiapt_BR
dc.contributor.departmentDepartamento de Farmacologiapt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.identifier.source000353787300004-
dc.creator.orcid0000-0001-9443-718Xpt_BR
dc.creator.orcid0000-0002-9482-6799pt_BR
dc.creator.orcid0000-0002-8449-6677pt_BR
dc.creator.orcid0000-0003-2201-8247pt_BR
dc.type.formArtigo original-
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