Objective To investigate the effect of captopril on expression of endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) in spontaneously hypertensive rats. Methods WKY (Wistar Kyoto) rats were used as the blank control. Spontaneous hypertensive rats(SHR) were used as the model group. SHR aged 7 ~ 24 weeks were administered captopril (3. 375 g / (kg·d)) and observed at 32 weeks. Blood pressure, left ventricular mass index (LVMI), aortic diastolic function, serum nitrite ion (NO₂ - ), and mRNA and protein contents of iNOS and eNOS were measured. Results (1) The left ventricular mass index and serum NO₂ - concentration of SHR were higher than those of WKY rats at various weeks and relaxation of the aorta was significantly lower than in WKY rats. (2) mRNA expression changes: compared with WKY rats, mRNA expression of eNOS and iNOS in the myocardium and arteries of SH rats were higher at various weeks, among which the maximum value of eNOS / iNOS appeared at 18 weeks. After administration of captopril, mRNA expression of iNOS and eNOS in the myocardium and arteries was significantly reduced at 24 and 32 weeks. (3) Protein expression changes: compared with WKY rats, the iNOS protein content in the myocardium and arteries of 18 and 24 weeks SHR were increased significantly, and that of 24 weeks SHR and 18 and 24 weeks SHR was increased significantly. Protein expression of iNOS in arteries was significantly reduced at 18 and 24 weeks by captopril and the effect disappeared after discontinuation. iNOS protein expression was significantly reduced at 24 and 32 weeks. Additionally, at 32 weeks, eNOS protein expression was significantly reduced in arteries and increased in the myocardium. Conclusions The pathological state of hypertension can lead to overexpression of iNOS and eNOS, and accumulation of iNOS and eNOS affects the occurrence of hypertension. Along with the pathogenesis of SHR hypertension, the nitric oxide system has a certain correlation with left ventricular hypertrophy and endothelial function. Captopril inhibits the expression of iNOS and eNOS in vivo to a certain extent and improves the left ventricular fat thickness and endothelial function.