Regulation of endothelial derived nitric oxide in health and disease
Mem. Inst. Oswaldo Cruz
;
100(supl.1): 15-18, Mar. 2005.
Article
in English
| LILACS
| ID: lil-402170
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.
Full text:
Available
Index:
LILACS (Americas)
Main subject:
Arteriosclerosis
/
Endothelium, Vascular
/
Diabetes Mellitus
/
Nitric Oxide Synthase Type III
/
Liver Cirrhosis
/
Nitric Oxide
Limits:
Animals
/
Humans
Language:
English
Journal:
Mem. Inst. Oswaldo Cruz
Journal subject:
Tropical Medicine
/
Parasitology
Year:
2005
Type:
Article
Affiliation country:
United States
Institution/Affiliation country:
Yale University/US
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