Reductions in nitric oxide (NO)activity persist after arterial intimal injury and may be a factor in the development of atherosclerosis. NO inhibits in vitro or in vivo platelet aggregation,leukocyte adhesion,and smooth muscle cell growth,all of which are key components in the process of intimal hyperplasia. We hypothesised that supplementation with Larginine, the presursor of NO, would increase NO production and thereby improve endothelium-dependent vasorelaxation and inhibit the development of atherosclerosis. Twenty-four New zealand white male rabbits were divided to four groups: ①uninjury, ②unilateral iliac artery injury + 2% cholesterol, ③ LArginine, ④unilateral iliac artery injury + 2% cholesterole 2K L-arginine. The iliac arteries were harvested for functional and morphometric studies. Maximal endothelium-dependent vasorelaxation in group ①,③and ④ was significantly greater than in group ②, but there was no significant difference of endothelium-dependent vasorelaxation among group ①, ③ and ④, L-arginine could partly inhibit the development of atheroselerotic plaques. These data suggest that L-arginine supplementation enhances NO production at sites of vascular healing and may reduce the development of proliferative atherosclerotic lesions.