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Local renin-angiotensin system regulates left ventricular hypertrophy induced by swimming training independent of circulating renin: a pharmacological study

Laboratory of Biochemistry, School of Physical Education and Sport, University of São Paulo, São Paulo, SP, Brazil, edilamar{at}usp.br

Maurício S. Sasaki

Laboratory of Biochemistry, School of Physical Education and Sport, University of São Paulo, São Paulo, SP, Brazil

Marcela Cerêncio

Laboratory of Biochemistry, School of Physical Education and Sport, University of São Paulo, São Paulo, SP, Brazil

Valério G. Baraúna

Laboratory of Biochemistry, School of Physical Education and Sport, University of São Paulo, São Paulo, SP, Brazil

José E. Krieger

Laboratory of Genetics and Molecular Cardiology, Heart Institute (InCor), University of São Paulo School of Medicine, São Paulo, SP, Brazil

Introduction.This study addressed the role of the local renin-angiotensin system (RAS) in the left ventricular hypertrophy (LVH) induced by swimming training using pharmacological blockade.

Materials and methods. Female Wistar rats treated with enalapril maleate (60 mg.kg^-1.d ^-1, n=38), losartan (20 mg.kg^-1.d^-1, n=36) or high salt diet (1% NaCl, n=38) were trained by two protocols (T1: 60-min swimming session, 5 days per week for 10 weeks and T2: the same T1 protocol until the 8^th week, then 9^th week they trained twice a day and 10^th week they trained three times a day). Salt loading prevented activation of the systemic RAS. Haemodynamic parameters, soleus citrate synthase (SCS) activity and LVH (left ventricular/body weight ratio, mg/g) were evaluated.

Results. Resting heart rate decreased in all trained groups. SCS activity increased 41% and 106% in T1 andT2 groups, respectively. LVH was 20% and 30% in T1 andT2 groups, respectively. Enalapril prevented 39% of the LVH in T2 group (p<0.05). Losartan prevented 41% in T1 and 50% inT2 (p<0.05) of the LVH in trained groups. Plasma renin activity (PRA) was inhibited in all salt groups and it was increased in T2 group.

Conclusions.These data provide evidence that the physiological LVH induced by swimming training is regulated by local RAS independent from the systemic, because the hypertrophic response was maintained even when PRA was inhibited by chronic salt loading. However, other systems can contribute to this process.

Key Words: enalapril maleate • exercise training • losartan • physiological cardiac hypertrophy • renin-angiotensin system

Journal of Renin-Angiotensin-Aldosterone System, Vol. 10, No. 1, 15-23 (2009)
DOI: 10.1177/1470320309102304


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