L-Arginine improves vascular function by overcoming deleterious effects of ADMA, a novel cardiovascular risk factor.
There is abundant evidence that the endothelium plays a crucial role in the maintenance of vascular tone and structure. One of the major endothelium-derived vasoactive mediators is nitric oxide (NO), an endogenous messenger molecule formed in healthy vascular endothelium from the amino acid precursor L-arginine. Endothelial dysfunction is caused by various cardiovascular risk factors, metabolic diseases, and systemic or local inflammation. One mechanism that explains the occurrence of endothelial dysfunction is the presence of elevated blood levels of asymmetric dimethylarginine (ADMA)--an L-arginine analogue that inhibits NO formation and thereby can impair vascular function. Supplementation with L-arginine has been shown to restore vascular function and to improve the clinical symptoms of various diseases associated with vascular dysfunction.
Böger
Rainer H
RH
Clinical Pharmacology Unit, Institute of Experimental and Clinical Pharmacology, Center of Experimental Medicine, University Hospital Hamburg-Eppendorf, Germany. boeger@uke.uni-hamburg.de.
Ron
Eyal S
ES
D001120:Arginine / Q000031:analogs & derivatives* / Q000378:metabolism / Q000627:therapeutic use*; D001161:Arteriosclerosis / Q000097:blood; D002318:Cardiovascular Diseases / Q000188:drug therapy / Q000209:etiology* / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism* / Q000502:physiology; D006801:Humans; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III
D009569:Nitric Oxide; C018524:N,N-dimethylarginine; D001120:Arginine; C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III