Aim To investigate the effectiveness of microRNA-195（miR-195）, transforming growth factor-β1/Smads（TGF-β1/Smads） signal transduction pathway and angiotensinⅡ（AngⅡ） in heart remodeling of spontaneously hypertensive rats （SHR）, and the impact of morphology and expression of the above factors for angiotensin-converting enzyme inhibitors（ACEI） drugs intervention on sp ontaneously hypertensive rats（SHR） heart. Methods 16 male SHRs and 8 male Wistar rats were recruited in this study. 16 male SHRs were randomly divided into benazepril treatment group（SHR treatment group,10mg/（kg·d）, n8） and control group（SHR control group,n8）. 8 Wistar rats were used as normal control group. What’s more, rats in SHR control group and normal control group were fed with distilled water, rats in SHR treatment group with gavage of benazepril 10 mg/（kg·d）. Eight weeks later, basal tail artery blood pressures of rats were measured. The morphologic changes of heart were examined with hemotoxylin and eosin（HE） staining.The expression of transforming growth factor beta1（TGF-β1）, angiotensin Ⅱ（AngⅡ）, small mother against decapentaplegic protein three（Smad3）, Collagen-Ⅰ（Col-Ⅰ） and Collagen-Ⅲ（Col-Ⅲ） proteins were detected by western blot. The expression of miRNA-195 were determined via Realtime polymerase chain reaction （qRT-PCR）. Results Compared to the normal control groups, the miRNA-195,AngⅡ,TGF-β1,Smad3,Col-Ⅰand Col-Ⅲ were higher expressed in SHR treatment group and SHR control groups（P<0.01 or P<0.05） Compared to the SHR control group, the cardiomyocyte of SB group becomes smaller and arranged more closely and orderly, the miRNA-195,AngⅡ,TGF-β1,Smad3,Col-Ⅰand Col-Ⅲ were significantly lower expressed（P<0.01 or P<0.05）. Conclusions MiRNA-195 may have a role to stop the progress of cardiac remodeling through up-regulation of AngⅡ and TGF-β1/Smads signal transduction pathway. The benazepril intervention may inhibit SHR cardiac remodeling as a result of inhibiting the expression of miRNA-195, through down-regulation of AngⅡ and TGF-β1/Smads signal transduction pathway.