New tricks from an old dog: nitric oxide-independent effects of dimethylarginine dimethylaminohydrolase

Leiper, J. and Vallance, P. (2006) New tricks from an old dog: nitric oxide-independent effects of dimethylarginine dimethylaminohydrolase. Arteriosclerosis, Thrombosis, and Vascular Biology, 26(7), pp. 1419-1420. (doi: 10.1161/01.ATV.0000229598.55602.17) (PMID:16794231)

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The enzyme dimethylarginine dimethylaminohydrolase (DDAH) metabolizes asymmetrically methylated arginine (namely L-N monomethylarginine [L-NMMA] and asymmetrical dimethylarginine [ADMA]) residues to citrulline and methylamine.1 Considerable interest has been focused on the biology of DDAH after the discovery that asymmetrically methylated arginines (in particular ADMA) are competitive inhibitors of all 3 isoforms of nitric oxide synthase (NOS).2 The observations that plasma ADMA levels are elevated in a range of cardiovascular disorders, some of which are associated with impaired NO generation, has led to the suggestion that inhibition of NOS activity by endogenously produced ADMA represents a novel mechanism to regulate NO production in vivo.3,4 Furthermore, it has been suggested that DDAH activity might be required to maintain ADMA levels below the concentration at which NOS inhibition would occur or might act to fine tune NOS activity by maintaining tonic inhibition of NOS3,4

Item Type:Articles
Glasgow Author(s) Enlighten ID:Leiper, Professor James
Authors: Leiper, J., and Vallance, P.
College/School:College of Medical Veterinary and Life Sciences > Institute of Cardiovascular and Medical Sciences
Journal Name:Arteriosclerosis, Thrombosis, and Vascular Biology
Publisher:American Heart Association
ISSN (Online):1524-4636
Published Online:22 June 2006

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