Vascular endothelial cell damage and excessive smooth muscle cell (SMC) proliferation are considered to paly a key role in the development of a atherosclerotic disease. In present study, it was Observed that nitric oxide-generating vasodilator-sodium nitroprosside (SNP) induced endothelium-independent relaxation on porcine coronary arterial rings and inhibited mitogenesis and proliferation of cultured procine vascular smooth muscle cells in dose-dependent manner with MTT colorimetric assay. The results suggest that endogenous nitric oxide (NO) may play an important role as medulator of smooth muscle cell growth, and the long-term administration of SNP and other nitrovasodilators which release NO in the body favors inhibiting the development of atherosclerosis to patients with atherosclerotic disease.