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This Article Full Text Full Text (PDF) All Versions of this Article: 295/2/R381    most recent 00933.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Barauna, V. G. Articles by Oliveira, E. M. Search for Related Content PubMed PubMed Citation Articles by Barauna, V. G. Articles by Oliveira, E. M.

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Control Mechanisms of Renin Synthesis and Release: A 21st Century Perspective

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

¹Laboratory of Biochemistry, School of Physical Education and Sports, University of São Paulo, São Paulo, ²Laboratory of Genetics and Molecular Cardiology and Unit of Applied Physiology, Heart Institute (InCor), University of São Paulo School of Medicine, São Paulo, Brazil

Submitted 31 December 2007 ; accepted in final form 19 May 2008

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 mg·kg^–1·day^–1, n = 6); trained + losartan (n = 6); control + high-salt diet (1%, n = 6); and trained + 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 MHC (-myosin heavy chain)-to-βMHC 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 ANG II concentration evaluated by ELISA remained unchanged (23.27 ± 2.4 vs. 22.01 ± 0.8 pg/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 AT₁ receptor expression with no changes in cardiac ANG II, which suggests a local activation of the RAS consistent with the hypertrophic response.

AT₁ receptor; renin-angiotensin system; cardiac hypertrophy; resistance training

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