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Am J Physiol Regul Integr Comp Physiol 278: R578-R586, 2000;
0363-6119/00 $5.00
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Vol. 278, Issue 3, R578-R586, March 2000

Myocardial renin is neither necessary nor sufficient to initiate or maintain ventricular hypertrophy

Stephen A. Katz1,2, John A. Opsahl3, Shane E. Wernsing3, Lynn M. Forbis2, Juline Smith4, and Lois J. Heller4

Departments of 1 Physiology and 3 Medicine, University of Minnesota Medical School, Minneapolis 55455; 2 Division of Nephrology, Hennepin County Medical Center, Minneapolis 55415; and 4 Department of Medical and Molecular Physiology, University of Minnesota School of Medicine, Duluth, Minnesota 55812

We tested the hypothesis that the myocardial renin-angiotensin system (RAS) is both necessary and sufficient to initiate and maintain all classes of ventricular hypertrophy. Myocardial and plasma renin and angiotensinogen were measured in rats during initiation and maintenance of ventricular hypertrophy associated with DOCA implants and 1% NaCl drinking water, with and without the AT1 ANG II receptor blocker losartan. Additional groups of rats were given a low-sodium diet (0.04%) for 3 wk. Ventricular hypertrophy was initiated within 7 days and maintained for 35 days in DOCA-treated rats despite significantly low myocardial and plasma renin, normal or low myocardial and plasma angiotensinogen, or the presence of losartan. Furthermore, there was no ventricular hypertrophy in low-salt diet-fed animals despite increased myocardial and plasma renin levels and normal angiotensinogen levels. Therefore, the myocardial RAS is not necessary to initiate or maintain cardiac hypertrophy in DOCA-treated rats and is not sufficient to initiate cardiac hypertrophy in low-salt diet-fed rats. Additionally, myocardial renin and angiotensinogen were significantly correlated with corresponding plasma levels.

renin-angiotensin system; losartan; cardiac growth; low-salt diet; deoxycorticosterone acetate


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