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Am J Physiol Regul Integr Comp Physiol 294: R26-R32, 2008. First published October 31, 2007; doi:10.1152/ajpregu.00424.2007
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Control Mechanisms of Renin Synthesis and Release: A 21st Century Perspective

The role of local and systemic renin angiotensin system activation in a genetic model of sympathetic hyperactivity-induced heart failure in mice

J. C. B. Ferreira,1 A. V. Bacurau,1 F. S. Evangelista,2 M. A. Coelho,1 E. M. Oliveira,1 D. E. Casarini,3 J. E. Krieger,2 and P. C. Brum1

1School of Physical Education and Sport, and 2Heart Institute (InCor), Medical School, University of São Paulo, and 3Nephrology Division, Federal University of Sao Paulo State, São Paulo, Brazil

Submitted 15 June 2007 ; accepted in final form 29 October 2007

Sympathetic hyperactivity (SH) and renin angiotensin system (RAS) activation are commonly associated with heart failure (HF), even though the relative contribution of these factors to the cardiac derangement is less understood. The role of SH on RAS components and its consequences for the HF were investigated in mice lacking {alpha}2A and {alpha}2C adrenoceptor knockout ({alpha}2A/{alpha}2CARKO) that present SH with evidence of HF by 7 mo of age. Cardiac and systemic RAS components and plasma norepinephrine (PN) levels were evaluated in male adult mice at 3 and 7 mo of age. In addition, cardiac morphometric analysis, collagen content, exercise tolerance, and hemodynamic assessments were made. At 3 mo, {alpha}2A/{alpha}2CARKO mice showed no signs of HF, while displaying elevated PN, activation of local and systemic RAS components, and increased cardiomyocyte width (16%) compared with wild-type mice (WT). In contrast, at 7 mo, {alpha}2A/{alpha}2CARKO mice presented clear signs of HF accompanied only by cardiac activation of angiotensinogen and ANG II levels and increased collagen content (twofold). Consistent with this local activation of RAS, 8 wk of ANG II AT1 receptor blocker treatment restored cardiac structure and function comparable to the WT. Collectively, these data provide direct evidence that cardiac RAS activation plays a major role underlying the structural and functional abnormalities associated with a genetic SH-induced HF in mice.

sympathetic nervous system; AT1 receptor blocker; {alpha}2a/{alpha}2c adrenergic knockout mice


Address for reprint requests and other correspondence: P. Chakur Brum, Escola de Educação Física e Esporte da Universidade de São Paulo, Departamento de Biodinâmica do Movimento do Corpo Humano, Av. Professor Mello Moraes, 65-Butantã-São Paulo-SP, CEP 05508-900 Brazil (e-mail: pcbrum{at}usp.br)




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