Captopril prevents vascular and fibrotic changes but not cardiac
hypertrophy in aortic-banded rats.
Regan, Christopher P., Peter G. Anderson, Sanford P. Bishop, Kathleen
H. Berecek.
Department of Physiology and Biophysics, University of Alabama at
Birmingham, Birmingham, AL 35294
APStracts 3:0080H, 1996.
To determine the role of the renin-angiotensin system (RAS) on
cardiovascular remodeling in a pressure overload model of cardiac
hypertrophy, a subdiaphragmatic aortic band was placed in adult,
male, Sprague Dawley rats. Rats were left untreated (AB), or given
captopril (Cap, 400mg/L) (AB-Cap). Sham-operated controls were either
left untreated (S) or given Cap (S-Cap). After 4 weeks, rats were
catheterized and carotid and femoral mean arterial pressures (CMAP
and FMAP in mmHg, respectively) recorded. Hearts were isolated and
minimal coronary resistance (MCR) determined. Hearts were then
perfusion-fixed, total and regional heart weights recorded, and
sections were processed for vessel morphology. Changes in coronary
artery medial thickness and perivascular fibrosis were assessed by
quantitative image analysis. CMAP was significantly higher in AB and
AB-Cap than S or S-Cap (p<0.05). There was no difference in FMAP
in AB vs. S, but AB-Cap and S-Cap had lower FMAP's than S. Total
heart weight and left ventricular weight / body weight ratios were
increased in AB and AB-Cap compared to S and S-Cap (p<0.05). MCR
of AB was greater than S and S-Cap. MCR of AB-Cap was significantly
greater than S and S-Cap but was significantly less than AB. In
coronary vessels, medial thickness was greatest in AB, while there
was no difference among AB-Cap, S, and S-Cap. Similarly, the increase
in perivascular fibrosis was greatest in AB and there was no
difference among AB-Cap, S, and S-Cap. These data suggest that the
RAS, independent of increased arterial pressure, is critical for the
development of the vascular and fibrotic changes that occur in this
model of pressure overload hypertrophy.
Received 18 October 1995; accepted in final form 8 February 1996.
APS Manuscript Number H970-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 March 96