title: Nitric oxide synthase: role in the genesis of vascular disease.
abstract: The product of nitric oxide (NO) synthase is the most potent endogenous vasodilator known. No not only is a potent vasodilator, it also inhibits platelet adherence and aggregation, reduces adherence of leukocytes to the endothelium, and suppresses proliferation of vascular smooth muscle cells. A number of disorders are associated with reduced synthesis and/or increased degradation of vascular NO. These include hypercholesterolemia, diabetes mellitus, hypertension, and tobacco use. The endothelial dysfunction caused by these disorders contributes to the alterations in vascular function and structure observed in these conditions. A reduction in the activity of vascular NO likely plays a significant role in the development of atherosclerosis. Insights into the mechanisms by which NO production or activity is altered in these states will lead to new therapeutic strategies in the treatment of a number of vascular disorders, including hypertension, atherosclerosis, restenosis, and thrombosis.
authors.affiliation: Division of Cardiovascular Medicine, Stanford University, California 94305, USA.
authors.forename: J P
authors.initials: JP
authors.lastname: Cooke
authors.forename: V J
authors.initials: VJ
authors.lastname: Dzau
mesh_terms: D000818:Animals; D001157:Arterial Occlusive Diseases / Q000503:physiopathology* / Q000628:therapy; D001161:Arteriosclerosis / Q000503:physiopathology* / Q000628:therapy; D004730:Endothelium, Vascular / Q000503:physiopathology; D006801:Humans; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000502:physiology*; D011379:Prognosis; D014655:Vascular Resistance / Q000502:physiology
chemical_list: D009569:Nitric Oxide; D019001:Nitric Oxide Synthase