title: ADMA and NOS regulation in chronic renal disease: beyond the old rivalry for l-arginine.
abstract: Chronic kidney disease is associated with increased levels of assymetric N(G),N(G)-dimethylarginine (ADMA), which is predictive of increased mortality and cardiovascular disease. ADMA induces endothelial dysfunction through competitive inhibition of the endothelial nitric oxide (eNOS) substrate L-arginine. Kajimoto et al. show that ADMA may also reduce nitric oxide production via decreased eNOS phosphorylation; this effect is mediated by the MAPK pathway and can be reversed in vivo by increased catabolism of ADMA through dimethylarginine dimethylaminohydrolase-1 overexpression.
authors.affiliation: Department of Physiological Sciences, Eastern Virginia Medical School, Norfolk, Virginia 23507, USA. dobriaad@evms.edu
authors.forename: Anca D
authors.initials: AD
authors.lastname: Dobrian
mesh_terms: D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood; D006801:Humans; D008297:Male; D052250:Nitric Oxide Synthase Type III / Q000037:antagonists & inhibitors*; D051436:Renal Insufficiency, Chronic / Q000503:physiopathology*
chemical_list: C018524:N,N-dimethylarginine; D001120:Arginine; D052250:Nitric Oxide Synthase Type III; C496315:Nos3 protein, mouse