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The cellular mechanisms leading to atherosclerosis are becoming more clearly defined. In response to hypercholesterolemia, an endothelial alteration or dysfunction occurs that precipitates monocyte adherence and infiltration. The specific alterations that lead to this initial event in atherogenesis are under intense study. A number of cytokines, adhesive molecules, and chemoattractants play an important role in this process. The reduced elaboration of antiatherogenic molecules may also be involved. Endothelium-derived relaxing factor, or nitric oxide, may be one such molecule. This substance, derived from the amino acid L-arginine, has potent antiplatelet and antiproliferative properties. More recently, it has been shown that this substance also inhibits interaction of leukocytes with the vessel wall. The influence of this factor is known to be reduced in hypercholesterolemic states, and this abnormality may promote atherogenesis. Restoration of nitric oxide activity appears to inhibit atherogenesis. This new finding may lead to new therapeutic approaches to atherosclerosis.
Cooke et al. (Thu,) studied this question.