Is atherosclerosis an arginine deficiency disease?
To conclude, an impairment of the NO synthase pathway may be one of the earliest events in atherogenesis. A reduction in NO synthesis and/or activity may contribute to the initiation and progressive of atherosclerosis. Derangement of the NO synthase pathway may occur by several mechanisms, including lipoproptein-induced alterations in signal transduction; increases in superoxide anion elaboration (and degradation of NO); reduced affinity of NOS for L-arginine; and/or elevated levels of circulating antagonists. NO is a potent vasodilator, a regulator of vascular structure, and an inhibitor of endothelial interactions and circulating blood elements. A loss of endothelial NO activity may contribute to the abnormal vasomotion observed in coronary artery disease, as well as the progression of atherosclerosis. Strategies to enhance NO synthesis and/or activity may be useful in maintaining cardiovascular health.
Cooke
J P
JP
Section of Vascular Medicine, Stanford University School of Medicine, CA 94305-5406, USA.
D000818:Animals; D001120:Arginine / Q000172:deficiency* / Q000502:physiology; D001161:Arteriosclerosis / Q000378:metabolism / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000503:physiopathology; D006801:Humans; D009569:Nitric Oxide / Q000502:physiology; D019001:Nitric Oxide Synthase / Q000502:physiology; D014664:Vasodilation / Q000502:physiology
D009569:Nitric Oxide; D001120:Arginine; D019001:Nitric Oxide Synthase