DDAH hydrolyzes both N(G),N(G)-dimethyl-L-arginine (ADMA) and N(G)-monomethyl-L-arginine (MMA), two nitric oxide synthase (NOS) inhibitors to yield L-citrulline and the corresponding alkylamine []. This way DDAH relieves the inhibition of NOS and promotes NO biosynthesis.There are two isoforms of DDHA, DDAH1 and DDAH2. DDAH1 predominates in tissues that express neuronal NOS [], but it is also important in vascular endothelial cells where it plays an important role in degrading the NOS inhibitors and regulating vascular tone [, ].
Mammalian dimethylarginine dimethylaminohydrolases DDAH1 and DDAH2 have homology with microbial arginine deiminases [], all of them are included in this entry.DDAH hydrolyzes both N(G),N(G)-dimethyl-L-arginine (ADMA) and N(G)-monomethyl-L-arginine (MMA), two nitric oxide synthase (NOS) inhibitors to yield L-citrulline and the corresponding alkylamine []. This way DDAH relieves the inhibition of NOS and promotes NO biosynthesis. Two isoforms exist, DDAH1 and DDAH2. DDAH1 predominates in tissues that express neuronal NOS []. DDAH2 expression predominates in highly vascularized tissues that express the endothelial NOS isoform and in immune tissues that can express iNOS [].
Dimethylarginine dimethylaminohydrolase (DDAH) modulates nitric oxide (NO) synthesis via metabolizing asymmetric dimethylarginine (ADMA), an endogenous NO synthase (NOS) inhibitor. Two isoforms of human dimethylarginine dimethylaminohydrolase exist, DDAH1 and DDAH2, with distinct tissue distributions. DDAH 1 predominates in tissues that express neuronal NOS []. DDAH2 expression predominates in highly vascularized tissues that express the endothelial NOS isoform and in immune tissues that can express iNOS [, ].
