The cardiac hypertrophy induced by anabolic steroid associated with the swimming training in rats: Involvement of the Renin Angiotensin Aldosterone System

Abstract

Experimental groups (n=56): Control (C), Anabolic Steroid (AS), AS+Losartan (AS+L), AS+Spironolactone (AS+S), Trained (T), Trained AS (TAS), Trained AS+Losartan (TAS+L) and Trained AS+Spironolactone (TAS+S). The AS was administered twice a week (10mg/kg/wk). The swimming training (ST) was performed for 10 weeks (5x/wk). The Losartan and Spironolactone were administered in drink water. AS induced cardiac hypertrophy (CH) in AS group compared to C group and it was increased in TAS group. AS treatment increased collagen volumetric fraction and collagen type III expression. The Losartan treatment inhibited the CH, but not Spironolactone. However, both treatments prevented cardiac collagen formation. AS groups increased the angiotensin converting enzyme (ACE) activity, AT1 and AT2 receptors expression. Treatment with Losartan or Spironolactone prevented the increase in ACE activity, but not AT1 and AT2 receptors expression. CYP11B2 expression was increased in TAS group and 11 βHSD2, TGFβ and osteopontin expression were increased in AS and TAS group. Both antagonists inhibited the AS effects and its association with ST. The results show the important participation of RAAS on CH induced by the association of AS and ST. For the first time we are showing the aldosterone (aldosterone synthase and 11β‐HSD2 expression) participation in these association.