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The role of asymmetric dimethylarginine (ADMA) in endothelial dysfunction and cardiovascular disease

Lookup NU author(s): Dr Latika Sibal, Dr Sharad Agarwal, Emeritus Professor Philip Home

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Abstract

Endothelium plays a crucial role in the maintenance of vascular tone and structure. Endothelial dysfunction is known to precede overt coronary artery disease. A number of cardiovascular risk factors, as well as metabolic diseases and systemic or local inflammation cause endothelial dysfunction. Nitric oxide (NO) is one of the major endothelium derived vaso-active substances whose role is of prime importance in maintaining endothelial homeostasis. Low levels of NO are associated with impaired endothelial function. Asymmetric dimethylarginine (ADMA), an analogue of L-arginine, is a naturally occurring product of metabolism found in human circulation. Elevated levels of ADMA inhibit NO synthesis and therefore impair endothelial function and thus promote atherosclerosis. ADMA levels are increased in people with hypercholesterolemia, atherosclerosis, hypertension, chronic heart failure, diabetes mellitus and chronic renal failure. A number of studies have reported ADMA as a novel risk marker of cardiovascular disease. Increased levels of ADMA have been shown to be the strongest risk predictor, beyond traditional risk factors, of cardiovascular events and all-cause and cardiovascular mortality in people with coronary artery disease. Interventions such as treatment with L-arginine have been shown to improve endothelium-mediated vasodilatation in people with high ADMA levels. However the clinical utility of modifying circulating ADMA levels remains uncertain. © 2010 Bentham Science Publishers Ltd.


Publication metadata

Author(s): Sibal L, Agarwal S, Home P, Boger R

Publication type: Review

Publication status: Published

Journal: Current Cardiology Reviews

Year: 2010

Volume: 6

Issue: 2

Pages: 82-90

Print publication date: 01/05/2010

ISSN (print): 1573-403X

ISSN (electronic): 1875-6557

URL: http://dx.doi.org/10.2174/157340310791162659

DOI: 10.2174/157340310791162659


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