Format

Send to

Choose Destination
See comment in PubMed Commons below
Int J Mol Sci. 2013 Dec 16;14(12):24412-21. doi: 10.3390/ijms141224412.

Biological functional relevance of asymmetric dimethylarginine (ADMA) in cardiovascular disease.

Author information

1
Department of Medicine and Science of Aging, University G. D'Annunzio-Chieti, Chieti 66100, Italy. l.speranza@unich.it.

Abstract

There is growing evidence that increased levels of the endogenous NO synthase inhibitor asymmetric dimethylarginine (ADMA) may contribute to endothelial dysfunction. Studies in animal models as well as in humans have suggested that the increase in ADMA occurs at a time when vascular disease has not yet become clinically evident. ADMA competitively inhibits NO elaboration by displacing L-arginine from NO synthase. In a concentration-dependent manner, it thereby interferes not only with endothelium-dependent, NO-mediated vasodilation, but also with other biological functions exerted by NO. The upshot may be a pro-atherogenic state. Recently, several studies have investigated the effect of various therapeutical interventions on ADMA plasma concentrations.

PMID:
24351825
PMCID:
PMC3876119
DOI:
10.3390/ijms141224412
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Multidisciplinary Digital Publishing Institute (MDPI) Icon for PubMed Central
    Loading ...
    Support Center