Figure 1.

Pathophysiological role of endothelium-derived nitric oxide (eNO) in atherosclerosis. Endothelium-derived NO is an antiatherogenic molecule synthesized from the precursor L-arginine in the presence of cofactors, cosubstrates, and NO synthase (eNOS). NOS is competitively inhibited by asymmetrical dimethylarginine (ADMA), an endogenous substrate for dimethylarginine dimethylaminohydrolase (DDAH). Uncoupling of eNOS favors the generation of proinflammatory reactive oxygen and nitrogen species that contribute to endothelial dysfunction and development of cardiovascular disease (CVD), including atherosclerosis.