Nitric oxide (NO) in the endothelium is synthesized by
endothelial nitric oxide synthase (eNOS) via the conversion
of L-arginine to L-citrulline. The reaction requires
the presence of the following cofactors: nicotinamide
adenine dinucleotide phosphate (NADPH), calcium/
calmodulin (CaM), flavin adenine dinucleotide (FAD), flavin
mononucleotide (FMN) and tetrahydrobiopterin (BH
4
).1,2
Nitric oxide has been recognized as a major antiatherogenic
factor because of its vasoprotective activity.3
Nitric oxide induces vasorelaxation by activating soluble
guanylate cyclase; thus, NO plays an important role in
regulating the vascular tone. Nitric oxide has also been
shown to inhibit oxidation of low-density lipoprotein (LDL)
and antagonize platelet aggregation by inhibiting platelet
activation.3 Moreover, NO inhibits nuclear factor-κBdependent
expression of adhesion molecules that mediate
recruitment of leukocytes to the endothelium in the early
phase of atherosclerosis. Nitric oxide has been shown to
suppress abnormal proliferation of vascular smooth muscle
cells, which contribute to the narrowing of atherosclerotic
vessel walls.3 Based on these anti-atherosclerotic properties,
the enhancement of endothelial NO production may
play an important role in the prophylaxis or treatment of
cardiovascular diseases.4