[ADMA (asymmetric dimethylarginine)--the inhibitor of nitric oxide (NO) synthesis: a new marker for vascular pathology].
Ample evidence is accumulating to suggest that asymmetric dimethylarginine (ADMA), an endogenous competitive inhibitor of nitric oxide synthase, is significantly elevated during phases of endothelial dysfunction. ADMA inhibits NO synthesis, hence its arterial infusion induces local arterial constriction. ADMA is generated ubiquitously in numerous tissues, by proteolysis of methylated proteins, while its degeneration is carried out mainly by the enzyme dimethylarginine dimethylaminohydrolase (DDAH). Administration of L-arginine can override partially NO synthesis by ADMA, yet it cannot eliminate the primary factors involved in the endothelial dysfunction. ADMA measurements might add valuable information about this new risk factor or at least a marker for adverse endothelial events.
Sela
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BA
The Institute for Chemical Pathology, Sheba Medical Center, Tel Hashomer. benamis@sheba.health.gov.il
D001120:Arginine / Q000031:analogs & derivatives* / Q000032:analysis / Q000494:pharmacology; D015415:Biomarkers / Q000032:analysis; D006801:Humans; D009569:Nitric Oxide / Q000037:antagonists & inhibitors* / Q000096:biosynthesis*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D014652:Vascular Diseases / Q000473:pathology*; D014661:Vasoconstriction / Q000187:drug effects*
D015415:Biomarkers; D009569:Nitric Oxide; C018524:N,N-dimethylarginine; D001120:Arginine; D019001:Nitric Oxide Synthase