Aim To investigate the effects and mechanism oframiprilat on c-myc expression induced by oxidized lowdensity lipoprotein (x-LDL) in vascular endothelialcells.Method After endothelial cells incubated with ox-LDL (250 mg/L) , ox-LDL+ramiprilat (20 mol/L) ,ox-LDL+ ramiprilat (40 mol/L) + N-Arg (1 00 mol/L ) , ox-LDL+N-Arg for 4 h in vitro. Reverse tran-scription PCR technique was employed to measure c-myc mRNA of cultured human umbilical vein endothe-lial cells (HUVEC). Nitric oxide (NO) and cGMPwere assayed by means of Griess reaction and radioim-munoassy respectively.Results in response to ox-LDL (250 mg/L) for 4 h,c-myc mRNA transcription of endothelial cells signifi-cantly increase (P<0. 05). In contrast , NO releaseand cGMP contents markedly decreased (P< 0. 05).Ramiprilat ( 20, 40 mol/L ) inhibited ox-LDL-in-duced c-myc expression and increased NO ,cGMP levelsof HUVEC. The effects of ramiprilat was partlyabolished by nitro-L-Arginine, a compeptitive in-hibitor of NO synthetase.Conclution Ramiprilat suppresses OLDL-induced c-myc overexpresion of endothelial cells by enhencingNO release.