Premium
AT1 receptor participates in resistance training induced cardiac hypertrophy in rats
Author(s) -
Oliveira Edilamar Menezes,
Barauna Valerio Garrone,
Rosa Kaleizu T,
Irigoyen Maria Claudia
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a344-a
Subject(s) - losartan , medicine , muscle hypertrophy , angiotensin ii receptor type 1 , endocrinology , angiotensin ii , ventricle , renin–angiotensin system , ejection fraction , receptor , heart failure , blood pressure
Besides the well‐known effects of ang II in stimulating pathological pressure‐overload cardiac hypertrophy, little information is available regarding the role of Renin‐Angiotensin‐System (RAS) in the exercise training‐induced cardiac hypertrophy. 35 male Wistar rats were divided in 4 groups: Sedentary (n=10); Trained (n=10); Sedentary + Losartan (20mg/Kg/d, n=7); Trained + Losartan (n=7). The exercise protocol was: 4 x 12 bouts, 5x/week during 8 weeks, with 65‐75% of 1 Repetition Maximum (1RM). Using LV weight/body weight ratio and echocardiography (ECHO) we have observed cardiac hypertrophy in Trained group without any impairment in ejection fraction, fractional shortening and E/A wave ratio. Concerning RAS, neither ACE, analyzed by fluorometric assay (systemic and local in the heart), nor Renin, by RIA, activities were altered after resistance training. In addition, using Western blotting analysis, no change was observed in cardiac Ang II and AT2 receptor levels while the AT1 receptor expression was upregulated in trained groups (13.4%). Administration of an AT1 receptor antagonist (losartan) using a subhypotensive dose prevented left ventricle hypertrophy in response to the resistance training. These results suggest that AT1 receptor participates in resistance‐training‐induced cardiac hypertrophy without the involvement of Ang II. A possible mechanism is direct activation of AT1 receptor by mechanical stretching of cardiomyocytes. Supported by Fapesp (n 04/11624‐6).