Aim To investigate the effects of captopril on vascular endothelial dysfunction induced by homocysteine thiolactone in rat in vivo.Methods The model of hyperhomocysteinemia(HHcy) in rats was induced by intragastric gavaged HTL,and the intervention groups were intragastric gavaged captopril in water.After treatment of 8 weeks,endothelium-dependent relaxation(EDR) of aortic rings were examined.Activity of paraoxonase1(PON1) and angiotensin-converting enzyme(ACE) in serum were analyzed.The masculine cell ratio of NF-κB P65 were detected by immunohistochemistry in vascular of rats.Results HTL significantly inhibited EDR induced by ACh,induced the activation of NF-κB P65 of vascular endothelium cell in rats;degraded the activity of PON1 and SOD in serum;down-regulated the PON1mRNA in the liver.Captopril could improve the EDR response and maintain the activity of PON1;up-regulated the PON1mRNA in the liver in dose-dependent manner.Captopril simultaneously inhibited the activation of NF-κB P65 of vascular endothelium cell in rats.Conclusion Captopril could protect vascular endothelial function induced by homocysteine thiolactone in rats.