CARDIAC HYPERTROPHY INDUCED BY SWIMMING TRAINING IS ASSOCIATED WITH ACTIVATION OF RENIN-ANGIOTENSIN SYSTEM

Abstract

635 Cardiac hypertrophy is one of the compensatories cardiovascular adaptations induced by exercise training (ET). Angiotensin II is a throphic factor which is involved in many cardiac hypertrophy models. In this study we evaluated the plasmatic and cardiac reninangiotensin system (RAS) components, during the cardiac hypertrophy development associated with swimming training in rats. We studied 16 male normotensive Wistar rats. Eigth were trained using a low-intensity swimming protocol for 8 weeks and 8 were kept sedentary. After ET arterial blood pressure (BP) was measured directly and tissue samples were extracted for morphometric and biochemical analysis. ACE activity was determined by fluorometric method using Hip-His-Leu as the substrate. Plasma renin activity (PRA) was evaluated by radioimunoassay (RIA). Results showed no changes in BP among the groups. The swimming training produced 13% hypertrophy of the left ventricle (LV) (1.95 vs. 2.2) and an increase in myocytes transversal diameter of 21% (10-13μm). Cardiac ACE activity increased 25% (1.7 vs. 2.2 nMol His-Leu/min/mg of protein) without changes in plasma (104.5 vs 111.5 nMol His-Leu/min/ml). The RPA increased 196% (0.4 vs. 1.3 ng Ang I/ml/h) in trained rats. These results suggested that swimming training induced cardiac hypertrophy and increased plasma renin and cardiac ACE activities indicating that systemic and local RAS may contribute to the development of this hypertrophy.