AT1 receptor participates in the cardiac hypertrophy induced by resistance gaining in rats

摘要

First published May 21, 2008; doi:10.1152/ajpregu.00933.2007.-Resistance training is accompanied by cardiac hypertrophy, but the role of the renin-angiotensin system (RAS) in this response is elusive. We evaluated this question in 36 male Wistar rats divided into six groups: control (n - 6); trained (n - 6); control + losartan (10 Dig-kg day~(-1), n - 6); trained + losartan (n = 6); control + high-salt diet (1%, n = 6); and trained 4- high-salt diet (1%, n = 6). High salt was used to inhibit the systemic RAS and losartan to block the AT1 receptor. The exercise protocol consisted of: 4 X 12 bouts, 5X/wk during 8 wk, with 65-75% of one repetition maximum. Left ventricle weight-to-body weight ratio increased only in trained and trained + high-salt diet groups (8.5% and 10.6%, P < 0.05) compared with control. Also, none of the pathological cardiac hypertrophy markers, atrial natriuretic peptide, and aMHC (alpha-myosin heavy chain)-to-3MHC ratio, were changed. ACE activity was analyzed by fluorometric assay (systemic and cardiac) and plasma renin activity (PRA) by RIA and remained unchanged upon resistance training, whereas PRA decreased significantly with the high-salt diet. Interestingly, using Western blot analysis and RT-PRC, no changes were observed in cardiac AT2 receptor levels, whereas the AT1 receptor gene (56%, P < 0.05) and protein (31%, P < 0.05) expressions were upregulated in the trained group. Also, cardiac ANGII concentration evaluated by ELISA remained unchanged (23.27 +- 2.4 vs. 22.01 +- 0.8pg/mg,P> 0.05). Administration of a subhypotensive dose of losartan prevented left ventricle hypertrophy in response to the resistance training. Altogether, we provide evidence that resistance training-induced cardiac hypertrophy is accompanied by induction of ATi receptor expression with no changes in cardiac ANG n, which suggests a local activation of the RAS consistent with the hypertrophic response.