Exercise training reduces cardiac angiotensin II levels and prevents cardiac dysfunction in a genetic model of sympathetic hyperactivity-induced heart failure in mice

Autor(es)

Pereira, M. G. ^[1] ; Ferreira, J. C. B. ^[1] ; Bueno, Jr., C. R. ^[1] ; Mattos, K. C. ^[1] ; Rosa, K. T. ^[2] ; Irigoyen, M. C. ^[2] ; Oliveira, E. M. ^[1] ; Krieger, J. E. ^[2] ; Brum, Patricia Chakur ^[3]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Sch Phys Educ & Sport, BR-05508900 Sao Paulo - Brazil

^[2] Univ Sao Paulo, Sch Med, Heart Inst InCor, BR-05508900 Sao Paulo - Brazil

^[3] Univ Sao Paulo, Dept Biodinam Movimento Corpo Humano, Escola Educ Fis & Esporte, BR-05508900 Sao Paulo - Brazil

• Tipo de documento: Artigo Científico
• Fonte: EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY; v. 105, n. 6, p. 843-850, APR 2009.
• Citações Web of Science: 44

Resumo

The role of exercise training (ET) on cardiac renin-angiotensin system (RAS) was investigated in 3-5 month-old mice lacking alpha(2A-) and alpha(2C-)adrenoceptors (alpha(2A)/alpha(2C)ARKO) that present heart failure (HF) and wild type control (WT). ET consisted of 8-week running sessions of 60 min, 5 days/week. In addition, exercise tolerance, cardiac structural and function analysis were made. At 3 months, fractional shortening and exercise tolerance were similar between groups. At 5 months, alpha(2A)/alpha(2C)ARKO mice displayed ventricular dysfunction and fibrosis associated with increased cardiac angiotensin (Ang) II levels (2.9-fold) and increased local angiotensin-converting enzyme activity (ACE 18%). ET decreased alpha(2A)/alpha(2C)ARKO cardiac Ang II levels and ACE activity to age-matched untrained WT mice levels while increased ACE2 expression and prevented exercise intolerance and ventricular dysfunction with little impact on cardiac remodeling. Altogether, these data provide evidence that reduced cardiac RAS explains, at least in part, the beneficial effects of ET on cardiac function in a genetic model of HF. (AU)

• Processo FAPESP: 06/57164-1 - Efeito do treinamento fisico aerobio sobre a via classica do sistema renina angiotensina na cardiomiopatia induzida por hiperatividade simpatica.
• Beneficiário: Marcelo Gomes Pereira
• Modalidade de apoio: Bolsas no Brasil - Mestrado
• Processo FAPESP: 05/59740-7 - Exercício físico e controle autonômico na fisiopatologia cardiovascular
• Beneficiário: Carlos Eduardo Negrão
• Modalidade de apoio: Auxílio à Pesquisa - Temático