Regulation of endothelial derived nitric oxide in health and disease.
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.
Sessa
William C
WC
Department of Pharmacology, Boyer Center for Molecular Medicine, School of Medicine, Yale University, New Haven, CT 06536-0812, USA. william.sessa@yale.edu
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*
D051242:Caveolin 1; D018841:HSP90 Heat-Shock Proteins; D009569:Nitric Oxide; D052250:Nitric Oxide Synthase Type III