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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampSilva, Gustavo henrique dapt_BR
dc.contributor.authorunicampSaad, Mário José Abdallapt_BR
dc.contributor.authorunicampHyslop, Stephenopt_BR
dc.contributor.authorunicampSalgado, Ionept_BR
dc.contributor.authorunicampHofling, Maria Alice da Cruzpt_BR
dc.typeArtigopt_BR
dc.titleHepatic morphological alterations, glycogen content and cytochrome P450 activities in rats treated chronically with N?-nitro-l-arginine methyl ester (l-name)pt_BR
dc.contributor.authorTarsitano, C.A.B.pt_BR
dc.contributor.authorDa Silva, G.H.pt_BR
dc.contributor.authorPaffaro, Jr. V.A.pt_BR
dc.contributor.authorPauli, J.R.pt_BR
dc.contributor.authorHyslop, S.pt_BR
dc.contributor.authorSaad, M.J.pt_BR
dc.contributor.authorDa Cruz,,Hofling M.A.pt_BR
dc.contributor.authorSalgado, I.pt_BR
unicamp.authorTarsitano, C.A.B., Departamento de Farmacologia, Faculdade de Ciências Médicas, Universidade Estadual de Campinas (UNICAMP), CP 6111, 13083-970 Campinas, SP, Brazil, Departamento de Biologia Celular e Estrutural, Instituto de Biologia, Universidade Estadual de Campinas (UNICAMP), CP 6109, 13083-970 Campinas, SP, Brazilpt_BR
unicamp.authorPaffaro Jr., V.A., Departamento de Histologia e Embriologia, Instituto de Biologia, Universidade Estadual de Campinas (UNICAMP), CP 6109, 13083-970 Campinas, SP, Brazilpt_BR
unicamp.authorPauli, J.R., Departamento de Clínica Médica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas (UNICAMP), CP 6111, 13083-970 Campinas, SP, Brazilpt_BR
unicamp.authorDa Silva, G.H., Departamento de Anatomia Patológica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas (UNICAMP), CP 6111, 13083-970 Campinas, SP, Brazilpt_BR
unicamp.authorSaad, M.J., Departamento de Clínica Médica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas (UNICAMP), CP 6111, 13083-970 Campinas, SP, Brazilpt_BR
unicamp.authorSalgado, I., Departamento de Bioquímica, Instituto de Biologia, Universidade Estadual de Campinas (UNICAMP), CP 6109, 13083-970 Campinas, SP, Brazilpt_BR
unicamp.authorDa Cruz-Höfling, M.A., Departamento de Histologia e Embriologia, Instituto de Biologia, Universidade Estadual de Campinas (UNICAMP), CP 6109, 13083-970 Campinas, SP, Brazilpt_BR
unicamp.authorHyslop, S., Departamento de Farmacologia, Faculdade de Ciências Médicas, Universidade Estadual de Campinas (UNICAMP), CP 6111, 13083-970 Campinas, SP, Brazilpt_BR
dc.subjectDoença crônicapt_BR
dc.subjectAtivação enzimáticapt_BR
dc.subjectInibidores enzimáticospt_BR
dc.subjectHipertensãopt_BR
dc.subjectHipertrofiapt_BR
dc.subject.otherlanguageChronic diseasespt_BR
dc.subject.otherlanguageEnzyme activationpt_BR
dc.subject.otherlanguageEnzyme inhibitorspt_BR
dc.subject.otherlanguageHypertensionpt_BR
dc.subject.otherlanguageHypertrophypt_BR
dc.description.abstractChronic treatment of rats with Nω-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) biosynthesis, results in hypertension mediated partly by enhanced angiotensin-I-converting enzyme (ACE) activity. We examined the influence of L-NAME on rat liver morphology, on hepatic glycogen, cholesterol, and triglyceride content, and on the activities of the cytochrome P450 isoforms CYP1A1/2, CYP2B1/2, CYP2C11, and CYP2E1. Male Wistar rats were treated with L-NAME (20 mg/rat per day via drinking water) for 2, 4, and 8 weeks, and their livers were then removed for analysis. Enzymatic induction was produced by treating rats with phenobarbital (to induce CYP2B1/2), β-naphthoflavone (to induce CYP1A1/2), or pyrazole (to induce CYP2E1). L-NAME significantly elevated blood pressure; this was reversed by concomitant treatment with enalapril (ACE inhibitor) or losartan (angiotensin II AT 1 receptor antagonist). L-NAME caused vascular hypertrophy in hepatic arteries, with perivascular and interstitial fibrosis involving collagen deposition. Hepatic glycogen content also significantly increased. L-NAME did not affect fasting glucose levels but significantly reduced insulin levels and increased the insulin sensitivity of rats, based on an intraperitoneal glucose tolerance test. Immunoblotting experiments indicated enhanced phosphorylation of protein kinase B and of glycogen synthase kinase 3. All these changes were reversed by concomitant treatment with enalapril or losartan. L-NAME had no effect on hepatic cholesterol or triglyceride content or on the basal or drug-induced activities and protein expression of the cytochrome P450 isoforms. Thus, the chronic inhibition of NO biosynthesis produced hepatic morphological alterations and changes in glycogen metabolism mediated by the renin-angiotensin system. The increase in hepatic glycogen content probably resulted from enhanced glycogen synthase activity following the inhibition of glycogen synthase kinase 3 by phosphorylation. © 2007 Springer-Verlag.en
dc.description.abstractChronic treatment of rats with N?-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) biosynthesis, results in hypertension mediated partly by enhanced angiotensin-I-converting enzyme (ACE) activity. We examined the influence of L-NAME on rat liver morphology, on hepatic glycogen, cholesterol, and triglyceride content, and on the activities of the cytochrome P450 isoforms CYP1A1/2, CYP2B1/2, CYP2C11, and CYP2E1. Male Wistar rats were treated with L-NAME (20 mg/rat per day via drinking water) for 2, 4, and 8 weeks, and their livers were then removed for analysis. Enzymatic induction was produced by treating rats with phenobarbital (to induce CYP2B1/2), ?-naphthoflavone (to induce CYP1A1/2), or pyrazole (to induce CYP2E1). L-NAME significantly elevated blood pressure; this was reversed by concomitant treatment with enalapril (ACE inhibitor) or losartan (angiotensin II AT 1 receptor antagonist). L-NAME caused vascular hypertrophy in hepatic arteries, with perivascular and interstitial fibrosis involving collagen deposition. Hepatic glycogen content also significantly increased. L-NAME did not affect fasting glucose levels but significantly reduced insulin levels and increased the insulin sensitivity of rats, based on an intraperitoneal glucose tolerance test. Immunoblotting experiments indicated enhanced phosphorylation of protein kinase B and of glycogen synthase kinase 3. All these changes were reversed by concomitant treatment with enalapril or losartan. L-NAME had no effect on hepatic cholesterol or triglyceride content or on the basal or drug-induced activities and protein expression of the cytochrome P450 isoforms. Thus, the chronic inhibition of NO biosynthesis produced hepatic morphological alterations and changes in glycogen metabolism mediated by the renin-angiotensin system. The increase in hepatic glycogen content probably resulted from enhanced glycogen synthase activity following the inhibition of glycogen synthase kinase 3 by phosphorylationpt
dc.relation.ispartofCell and tissue researchpt_BR
dc.relation.ispartofabbreviationCell tissue res.pt_BR
dc.publisher.cityNew York, NYpt_BR
dc.publisher.countryEstados Unidospt_BR
dc.publisherSpringer-Verlagpt_BR
dc.date.issued2007pt_BR
dc.identifier.citationCell And Tissue Research. , v. 329, n. 1, p. 45 - 58, 2007.pt_BR
dc.language.isoengpt_BR
dc.description.volume329pt_BR
dc.description.issuenumber1pt_BR
dc.description.firstpage45pt_BR
dc.description.lastpage58pt_BR
dc.rightsfechadopt_BR
dc.sourceScopuspt_BR
dc.sourceSCOPUSpt_br
dc.identifier.issn0302-766Xpt_BR
dc.identifier.eissn1432-0878pt_BR
dc.identifier.doi10.1007/s00441-007-0411-9pt_BR
dc.identifier.urlhttps://link.springer.com/article/10.1007%2Fs00441-007-0411-9pt_BR
dc.date.available2015-06-30T18:37:46Z
dc.date.available2015-11-26T15:01:28Z-
dc.date.accessioned2015-06-30T18:37:46Z
dc.date.accessioned2015-11-26T15:01:28Z-
dc.description.provenanceMade available in DSpace on 2015-06-30T18:37:46Z (GMT). No. of bitstreams: 1 2-s2.0-34247640715.pdf: 898947 bytes, checksum: 8e58af75897a681884ffcb8642d00518 (MD5) Previous issue date: 2007en
dc.description.provenanceMade available in DSpace on 2015-11-26T15:01:28Z (GMT). No. of bitstreams: 2 2-s2.0-34247640715.pdf: 898947 bytes, checksum: 8e58af75897a681884ffcb8642d00518 (MD5) 2-s2.0-34247640715.pdf.txt: 61626 bytes, checksum: 412045c713e8f48268f1eabac3c01b6d (MD5) Previous issue date: 2007en
dc.identifier.urihttp://www.repositorio.unicamp.br/handle/REPOSIP/104069
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/104069-
dc.identifier.idScopus2-s2.0-34247640715pt_BR
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dc.contributor.departmentDepartamento de Clínica Médicapt_BR
dc.contributor.departmentDepartamento de Farmacologiapt_BR
dc.contributor.departmentDepartamento de Bioquímicapt_BR
dc.contributor.departmentDepartamento de Histologia e Embiologiapt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeInstituto de Biologiapt_BR
dc.contributor.unidadeInstituto de Biologiapt_BR
dc.identifier.source2-s2.0-34247640715-
dc.creator.orcid0000-0002-1046-7646pt_BR
dc.creator.orcid0000-0003-4544-6105pt_BR
dc.creator.orcid0000-0003-4113-0189pt_BR
dc.type.formArtigo original-
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