(Hypertension. 1996;27:14-18.)
© 1996 American Heart Association, Inc.
Articles |
Chronic L-Arginine Administration Attenuates Cardiac Hypertrophy in Spontaneously Hypertensive Rats
From the Department of Internal Medicine III, Kurume University School of Medicine, and Kurume University Medical Center, Kurume, Japan.
Abstract Nitric oxide inhibits proliferation and migration of
vascular smooth muscle cells and contractility of
cardiomyocytes in vitro. In spontaneously hypertensive rats
(SHR), evidence suggests intrinsic abnormalities of the
L-arginine–nitric oxide axis, such as low
cGMP-dependent protein kinase in the heart and abnormal
L-arginine metabolism. To investigate the in
vivo effect of L-arginine on cardiac
hypertrophy, 30 SHR and 30 Wistar-Kyoto rats (WKY) were
randomly grouped to receive L-arginine (7.5 g/L in drinking
water) or vehicle for 12 weeks. L-Arginine treatment did
not affect body weight or arterial pressure in either
strain. In vehicle-treated animals, the heart/body weight ratio was
significantly higher in SHR than in WKY (P<.01).
L-Arginine treatment decreased the heart/body weight ratio
in SHR (P<.05) but did not affect it in WKY. Expression of
skeletal 
-actin mRNA, known to be expressed in the hypertrophied
myocardium, was attenuated in
L-arginine–treated SHR compared with
vehicle-treated SHR. Cardiac cGMP content and nitrate/nitrite
content were less in SHR than WKY. L-Arginine treatment
increased these levels only in SHR, suggesting enhanced nitric oxide
production. Thus, chronic L-arginine administration
attenuated cardiac hypertrophy independently of blood
pressure and increased myocardial content of cGMP and nitrate/nitrite.
Our results suggest that abnormality of the cardiac
L-arginine–nitric oxide axis may play an important
role in the pathogenesis of cardiac hypertrophy in SHR.
Key Words: -actin • cyclic GMP • nitric oxide • arginine • nitrates • heart hypertrophy
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