Nitric oxide synthase: role in the genesis of vascular disease.

Published

Journal Article (Review)

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.

Full Text

Duke Authors

Cited Authors

  • Cooke, JP; Dzau, VJ

Published Date

  • 1997

Published In

Volume / Issue

  • 48 /

Start / End Page

  • 489 - 509

PubMed ID

  • 9046979

Pubmed Central ID

  • 9046979

International Standard Serial Number (ISSN)

  • 0066-4219

Digital Object Identifier (DOI)

  • 10.1146/annurev.med.48.1.489

Language

  • eng

Conference Location

  • United States