Format

Send to

Choose Destination
See comment in PubMed Commons below
Mem Inst Oswaldo Cruz. 2005 Mar;100 Suppl 1:15-8. Epub 2005 Jun 14.

Regulation of endothelial derived nitric oxide in health and disease.

Author information

1
Department of Pharmacology, Boyer Center for Molecular Medicine, School of Medicine, Yale University, New Haven, CT 06536-0812, USA. william.sessa@yale.edu

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.

PMID:
15962093
DOI:
/S0074-02762005000900004
[Indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Scientific Electronic Library Online
    Loading ...
    Support Center