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NO is a potent vasodilator that activates soluble guanylate cyclase, thereby increasing intracellular levels of cyclic GMP. In addition, NO exerts an inhibitory influence on cell proliferation and adhesion. The proliferation of vascular smooth muscle cells or lymphocytes in culture is inhibited by exogenous NO donors as well as endogenous NO.Platelet adhesion and aggregation as well as monocyte adhesion and chemotaxis are negatively regulated by this molecule. These in vitro studies indicate that NO suppresses a number of key processes that are involved in atherogenesis. It seems logical, therefore, that a reduction in the activity of vascular NO would promote atherogenesis. Indeed, one of the earliest abnormalities to occur in hypercholesterolemic animals and humans is a reduction in the activity of vascular NO, as manifested by impaired endothelium-dependent vasodilation. This occurs well before any structural changes in the vessel wall. This impairment in endothelium-dependent vasodilation is reversible in hypercholesterolemic animal models and humans by intravenous infusion of the NO precursor L-arginine. The effect of L-arginine to normalize endothelium-dependent vasodilation is likely due to its metabolism to NO, since the effect is not mimicked by D-arginine (which is not a substrate for NO synthase).Chronic administration of supplemental dietary arginine to hypercholesterolemic rabbits is also associated with an improvement in endothelium-dependent vasodilation. The sustained enhancement of vascular NO activity is paralleled by a striking inhibition of intimal lesion formation in these animals. Dietary arginine also exerts an inhibitory effect on neointimal lesion formation after balloon injury in this animal

Is NO an endogenous antiatherogenic molecule?