Memórias do Instituto Oswaldo Cruz
Fundação Oswaldo Cruz, Fiocruz
Vol. 100, No. s1, 2005, pp. 15-18
Bioline Code: oc05021
Full paper language: English
Document type: Research Article
Document available free of charge
Memórias do Instituto Oswaldo Cruz, Vol. 100, No. s1, 2005, pp. 15-18
© Copyright 2005 - Instituto Oswaldo Cruz - Fiocruz.
Regulation of endothelial derived nitric oxide in health and disease|
William C Sessa
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.
nitric oxide - endothelium - caveolin-1 - heat shock protein 90 - atherosclerosis - inflammation
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