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1 Cardiovascular Research and 2 Department of Pharmacology, Berlex Biosciences, Richmond, California 94804-0099
This study
investigated the role of endogenous nitric oxide (NO) in the
progression of atherosclerosis in apolipoprotein E-deficient [apoE-knockout (KO)] mice. Mice were treated with
N
-nitro-L-arginine methyl ester
(L-NAME) an inhibitor of nitric oxide synthase (NOS) or
with the NOS substrate L-arginine for 8 wk.
L-NAME treatment resulted in a significant inhibition of NO-mediated vascular responses and a significant increase in the atherosclerotic plaque/surface area in the aorta of apoE-KO mice. L-arginine treatment had no influence on endothelial
function and did not alter lesion size. Mean arterial blood pressure
and serum lipid levels were not altered by the treatments. At the beginning of the study impairment in endothelial function was only
apparent in the case of
NG-nitro-L-arginine-induced,
NO-mediated contraction, whereas ACh-induced, NO-mediated relaxation
was not different between age-matched apoE-KO and C57Bl/6J mice. After
the 8-wk treatment with the NOS inhibitor, both NO-mediated responses
were significantly inhibited. The acceleration in lesion size
concomitant to the severely impaired NO-mediated responses indicates
that lack of endogenous NO is an important progression factor of
atherosclerosis in the apoE-KO mouse.
endothelium; plaque development and progression; L-arginine; N-nitro-L-arginine methyl
ester
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