Angiotensin receptor 1 blockade does not prevent physiologic
cardiac hypertrophy in the adult rat.
Geenen, David L., Ashwani Malhotra, and Peter M. Buttrick.
Division of Cardiology, Albert Einstein College of Medicine /
Montefiore Medical Center, Bronx, NY
APStracts 3:0206A, 1996.
The renin-angiotensin system (RAS) has been implicated in the
hypertrophic adaptation of the heart to exogenous pathologic loads,
such as hypertension and aortic stenosis, however the role of this
hormonal system in the cardiac adaptations to physiologic loads, such
as chronic exercise conditioning has not been established. We
therefore studied the effect of angiotensin receptor 1 (AT1) blockade
on the chronic cardiac responses of rats subjected to an eight week
swimming program. Compared to matched sedentary controls, untreated
swimmers increased their left ventricular weights (LV) by 13% and
swimmers treated with the AT1 antagonist, L-158,809, increased their
LV weights by 11% (both p < 0.05 vs sedentary controls). The
incorporation of labeled amino acids into the heart at the time of
sacrifice was unchanged in all groups and therefore the increase in
heart weight in both swim conditioned groups appeared to reflect a
decrease in the rate of protein degradation in the heart. Hearts from
both swim conditioned groups manifested an increase in the V1
predominant myosin isoform pattern but not an increase in atrial
natriuretic factor (ANF) mRNA expression or protein kinase C
translocation. The fact that these patterns of adaptation are
preserved in exercised conditioned animals treated with an AT1
antagonist suggests that the chronic hypertrophic response of the
heart to physiologic loads is not influenced by the RAS.
Received 21 August 1995; accepted in final form 22 March 1996.
APS Manuscript Number A916-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 1 May 96