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.
|Original language||English (US)|
|Number of pages||4|
|Journal||Journal of Investigative Medicine|
|State||Published - Jan 1 1998|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)