Aim To observe the expressions of endothelin-1 (ET-1), nitric oxide (NO) and nitric oxide synthase (NOS) in the anoxia-reoxygenation (H/R) injury on human umbilical vein endothelial cells (EC), and further research the molecular mechanism of catopril late effect on production of ET-1 and NO. Methods The third passage of cultured EC was randomly divided into 7 groups: control, anoxia, anoxia-reoxygenation, catopril, catopril+bradykinin Β 2 receptor inhibitor, catopril+PKC inhibitor, catopril+NF-κB inhibitor. Total RNA was extracted. The expression of ET-1, endthelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) mRNA were analyzed by semi-quantiative RT-PCR method. The protein level of total NOS and NO were analyzed too. Results ET-1 mRNA expression increased significantly in anoxia group and anoxia-reoxygenation group, decreased in catopril group, and increased in three inhibitor groups. While the mRNA expressions of iNOS and eNOS were contrary to that of ET-1, and the change of iNOS was slightly. The protein levels of total NOS and NO are lower in anoxia group and anoxia-reoxygenation group than in control group, higher in catopril group than in anoxia group or anoxia-reoxygenation group, and lower in three inhibitor groups than in catopril group, but higher than in anoxia-reoxygenation group. Conclusion Anoxia-reoxygenation injury can induce ET-1 expression increasing and NO expression decreasing. Catopril can protect the imbalance of ET-1 and NO. Bradykinin Β 2 receptor, PKC activating and nucleus factor are partly involved in the protective effect.