title: Regulation of endothelial derived nitric oxide in health and disease.
abstract: Endothelial nitric oxide synthase (eNOS) is the primary physiological source of nitric oxide (NO) that regulates cardiovascular homeostasis. Historically eNOS has been thought to be a constitutively expressed enzyme regulated by calcium and calmodulin. However, in the last five years it is clear that eNOS activity and NO release can be regulated by post-translational control mechanisms (fatty acid modification and phosphorylation) and protein-protein interactions (with caveolin-1 and heat shock protein 90) that direct impinge upon the duration and magnitude of NO release. This review will summarize this information and apply the post-translational control mechanisms to disease states.
authors.affiliation: Department of Pharmacology, Boyer Center for Molecular Medicine, School of Medicine, Yale University, New Haven, CT 06536-0812, USA. william.sessa@yale.edu
authors.forename: William C
authors.initials: WC
authors.lastname: Sessa
mesh_terms: D000818:Animals; D001161:Arteriosclerosis / Q000378:metabolism*; D051242:Caveolin 1 / Q000502:physiology; D003920:Diabetes Mellitus / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000378:metabolism*; D004789:Enzyme Activation; D018841:HSP90 Heat-Shock Proteins / Q000502:physiology; D006801:Humans; D008103:Liver Cirrhosis / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism*
chemical_list: D051242:Caveolin 1; D018841:HSP90 Heat-Shock Proteins; D009569:Nitric Oxide; D052250:Nitric Oxide Synthase Type III