Nitric oxide is formed from the N-guanido terminal of the amino acid L-argi
nine and from molecular oxygen by nitric oxide synthase enzymes. L-arginine
administration improves the coronary blood flow response to acetylcholine
in patients with normal coronary arteries and hypercholesterolemia, reverse
s the defective endothelium-dependent vasodilation associated with an eleva
ted plasma low-density lipoprotein level or hypercholesterolemia, dilates c
oronary epicardial arteries and stenoses, enhances nitric oxide generation,
and inhibits lesion formation after balloon angioplasty. Stimulation of en
dogenous nitric oxide production could inhibit atherogenesis, and therefore
may be of benefit in patients with risk factors for atherosclerosis. (C) 2
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