Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/37781
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dc.contributor.authorGomes-Santos, Igor Lucas
dc.contributor.authorFernandes, Tiago
dc.contributor.authorCouto, Gisele Kruger
dc.contributor.authorAyres Ferreira-Filho, Julio Cesar
dc.contributor.authorCury Salemi, Vera Maria
dc.contributor.authorFernandes, Fernanda Barrinha [UNIFESP]
dc.contributor.authorCasarini, Dulce Elena [UNIFESP]
dc.contributor.authorBrum, Patricia Chakur
dc.contributor.authorRossoni, Luciana Venturini
dc.contributor.authorOliveira, Edilamar Menezes de
dc.contributor.authorNegrao, Carlos Eduardo
dc.date.accessioned2016-01-24T14:37:18Z-
dc.date.available2016-01-24T14:37:18Z-
dc.date.issued2014-05-23
dc.identifierhttp://dx.doi.org/10.1371/journal.pone.0098012
dc.identifier.citationPlos One. San Francisco: Public Library Science, v. 9, n. 5, 11 p., 2014.
dc.identifier.issn1932-6203
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/37781-
dc.description.abstractBackground: Accumulated evidence shows that the ACE-AngII-AT1 axis of the renin-angiotensin system (RAS) is markedly activated in chronic heart failure (CHF). Recent studies provide information that Angiotensin (Ang)-(1-7), a metabolite of AngII, counteracts the effects of AngII. However, this balance between AngII and Ang-(1-7) is still little understood in CHF. We investigated the effects of exercise training on circulating and skeletal muscle RAS in the ischemic model of CHF.Methods/Main Results: Male Wistar rats underwent left coronary artery ligation or a Sham operation. They were divided into four groups: 1) Sedentary Sham (Sham-S), 2) exercise-trained Sham (Sham-Ex), sedentary CHF (CHF-S), and exercise-trained CHF (CHF-Ex). Angiotensin concentrations and ACE and ACE2 activity in the circulation and skeletal muscle (soleus and plantaris) were quantified. Skeletal muscle ACE and ACE2 protein expression, and AT1, AT2, and Mas receptor gene expression were also evaluated. CHF reduced ACE2 serum activity. Exercise training restored ACE2 and reduced ACE activity in CHF. Exercise training reduced plasma AngII concentration in both Sham and CHF rats and increased the Ang-(1-7)/AngII ratio in CHF rats. CHF and exercise training did not change skeletal muscle ACE and ACE2 activity and protein expression. CHF increased AngII levels in both soleus and plantaris muscle, and exercise training normalized them. Exercise training increased Ang-(1-7) in the plantaris muscle of CHF rats. the AT1 receptor was only increased in the soleus muscle of CHF rats, and exercise training normalized it. Exercise training increased the expression of the Mas receptor in the soleus muscle of both exercise-trained groups, and normalized it in plantaris muscle.Conclusions: Exercise training causes a shift in RAS towards the Ang-(1-7)-Mas axis in skeletal muscle, which can be influenced by skeletal muscle metabolic characteristics. the changes in RAS circulation do not necessarily reflect the changes occurring in the RAS of skeletal muscle.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipFundacao Zerbini
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.format.extent11
dc.language.isoeng
dc.publisherPublic Library Science
dc.relation.ispartofPlos One
dc.rightsAcesso aberto
dc.titleEffects of Exercise Training on Circulating and Skeletal Muscle Renin-Angiotensin System in Chronic Heart Failure Ratsen
dc.typeArtigo
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.description.affiliationUniv São Paulo, Sch Med, Heart Inst InCor HCFMUSP, São Paulo, Brazil
dc.description.affiliationUniv São Paulo, Sch Phys Educ & Sport, São Paulo, Brazil
dc.description.affiliationUniv São Paulo, Inst Biomed Sci, Dept Physiol & Biophys, São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Kidney & Hypertens Hosp, Div Nephrol, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Kidney & Hypertens Hosp, Div Nephrol, São Paulo, Brazil
dc.description.sponsorshipIDFAPESP: FAPESP-2010/50048-1
dc.identifier.fileWOS000336839400034.pdf
dc.identifier.doi10.1371/journal.pone.0098012
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000336839400034
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