Caracterização da participação do sistema renina-angiotensina na cardiomiopatia induzida por hiperatividade simpática / Characterization of renin-angiotensin system in cardiomyopathy induced by sympathetic hyperactivity

AUTOR(ES)
DATA DE PUBLICAÇÃO

2006

RESUMO

We have recently reported that disruption of both alfa2A and alfa2C adrenergic receptor subtypes (KO) in mice leads to sympathetic hyperactivity with evidence of heart failure (HF) by seven months (mo) of age. In the present study, we have performed the phenotypical characterization on KO mice at three and seven month of age. In addition, we evaluated the effect of sympathetic hyperactivity on cardiac renin-angiotensin system (RAS) components. For that, we evaluated cardiac Ang II content, angiotensin converting activity (ACE), plasma renin activity and cardiac angiotensinogen expression. At three mo, KO mice displayed reduced fractional shortening (16%) and increased cardiomyocyte width compared with age-matched wild type (WT). Indeed, KO mice showed significantly increased cardiac Ang II content, cardiac ACE activity, angiotensinogen expression and plasma renin activity. At seven mo, KO mice displayed exercise intolerance, reduced fractional shortening (34%), cardiac dilatation, lung edema, increased cardiomyocyte width and increased cardiac collagen content compared with age-matched WT. In addition, KO mice presented an increased cardiac Ang II content and angiotensinogen expression, concomitantly with a decreased plasma renin activity. Collectively, these results uncover potential feedback regulation of cardiac and circulating components of SNS and RAS, which may contribute to a better understanding of the processes taking place during the progression of cardiomyopathy induced by sympathetic hyperactivit.

ASSUNTO(S)

heart failure camundongos geneticamente modificados insuficiência cardíaca renin angiotensin system sympathetic nervous system sistema nervoso simpático sistema renina-angiotensina

ACESSO AO ARTIGO

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