L-Arginine is the substrate of endothelial nitric oxide synthase and the
main precursor of nitric oxide in the vascular endothelium, thus its
effects are mediated largely by increases in nitric oxide production.
L-Arginine has antioxidant and antiapoptotic properties, increases
smooth muscle relaxation, inhibits the expression of adhesion molecules
and chemotactic peptides, decreases endothelin-1 expression, and
inhibits platelet aggregation. This amino acid also improves endothelial
function in patients with coronary artery disease and dilates human
epicardial atheromatous coronary arteries. Despite the positive results
from small case - control studies, it is still unclear whether chronic
administration of L-arginine has any effect on clinical outcome in
patients with coronary artery disease. In addition, other indirect
strategies, such as the inhibition of arginase, could prove more
effective at improving intracellular L-arginine bioavailability than
exogenous L-arginine administration. The potential clinical usefulness
of L-arginine, therefore, needs further evaluation in large, prospective
clinical trials. Here, we present a critique of the existing literature
about the role of L-arginine in the prevention of atherosclerosis