(Hypertension. 1997;30:1621-1627.)
© 1997 American Heart Association, Inc.
Articles |
Chronic Angiotensin-Converting Enzyme Inhibition and Angiotensin II Type 1 Receptor Blockade
Effects on Cardiovascular Remodeling in Rats Induced by the Long-term Blockade of Nitric Oxide Synthesis
From the Research Institute of Angiocardiology and Cardiovascular Clinic (M.T., K.E., H.T., M.U., H.S., A.T.) and the First Department of Pathology (K.S.), Kyushu University School of Medicine, Fukuoka, Japan, and the Department of Cardiovascular Medicine (H.O., A.K.), Hokkaido University School of Medicine, Sapporo, Japan.
Correspondence to Kensuke Egashira, MD, PhD, Research Institute of Angiocardiology and Cardiovascular Clinic, Kyushu University School of Medicine 3-1-1, Maidashi, Higashi-ku, Fukuoka 812-82, Japan. E-mail egashira{at}cardiol.med.kyushu-u.ac.jp
Abstract We have shown previously that
angiotensin-converting enzyme (ACE) inhibitors
prevent coronary vascular remodeling (medial thickening and
perivascular fibrosis) and myocardial remodeling (fibrosis and
hypertrophy) in rats induced by long-term inhibition of
nitric oxide (NO) synthesis with oral administration of
N
-nitro-L-arginine methyl
ester (L-NAME). ACE inhibitors inhibit both the formation
of angiotensin II and the catabolism of bradykinin. In this
study, we aimed to determine the relative contribution of the latter
two mechanisms to the beneficial effects of an ACE
inhibitor on structural remodeling. First, we examined the
effects of the ACE inhibitor temocapril and the
angiotensin II AT1 subtype receptor
antagonist CS-866 on the structural remodeling induced by
administering L-NAME for 8 weeks. Temocapril and CS-866 were equally
effective in preventing remodeling. Second, we examined whether the
effect of temocapril on the remodeling induced by L-NAME was reduced by
the bradykinin receptor antagonist HOE140. The latter drug
did not alter the beneficial effect of temocapril on remodeling. In
conclusion, although species differences must be considered to apply
our conclusion to clinical conditions, the present results suggest
that the inhibition of angiotensin II activity, mediated
via the AT1 receptors, is responsible for the beneficial
effects of an ACE inhibitor in our animal model of
coronary vascular and myocardial remodeling induced by the
long-term inhibition of NO synthesis.
Key Words: angiotensin • endothelium-derived factors • bradykinin • collagen hypertrophy • remodeling
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