Regulation of endothelial derived nitric oxide in health and disease
AUTOR(ES)
Sessa, William C
FONTE
Memórias do Instituto Oswaldo Cruz
DATA DE PUBLICAÇÃO
2005-03
RESUMO
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.
Documentos Relacionados
- The effect of nitric oxide, endothelial nitric oxide synthetase, and asymmetric dimethylarginine in hemorrhoidal disease
- Sepiapterin reductase regulation of endothelial tetrahydrobiopterin and nitric oxide bioavailability
- Endothelial nitric oxide synthase immunoreactivity in early gestation and in trophoblastic disease.
- Regulation of bovine endothelial constitutive nitric oxide synthase by oxygen.
- Regulation of nitric oxide synthesis by proinflammatory cytokines in human umbilical vein endothelial cells. Elevations in tetrahydrobiopterin levels enhance endothelial nitric oxide synthase specific activity.
