Abstract: AIM To explore the role and mechanisms of miR-26a/b in cardiac remodeling after hypertension. METHODS The present investigation utilized 12 male C57 mice as experimental subjects, which were randomly divide into two groups, an experimental group and a control group. The hypertension cardiac remodeling model was induced by continuously infused Ang. Parts of mice's hearts were made into paraffin-embedded sections to observe the changes of heart shape, size and fibrosis of myocardial cells via HE and Masson staining. The expression levels of CTGF, Collagen Ⅰ, Collagen Ⅲ and fibronectin protein in mouse heart tissue were evaluated using Western blot. Expression levels of miR-26a/b in mouse heart tissue and blood serum were evaluated using real-time PCR. RESULTS After cardiac remodeling, fibrosis tissues between cells and around small vessels increased in the experimental group. In the experimental group, the expression of CTGF, Collagen Ⅰ, Collagen Ⅲ and fibronectin protein were up-regulated significantly (P<0.05, P<0.01). Expression of miR-26a/b was significantly down-regulated in heart tissues and blood serum (P<0.05, P<0.01). CONCLUSION Continuous infusion of AngⅡ significantly down-regulates the expression of miR-26a/b in the heart and up-regulates the expressions of CTGF, Collagen I, Collagen I and fibronectin, indicating that AngⅡ is involved in hypertension cardiac remodeling and down-regulates the expression of miR-26a/b. MiRNA-26a/b in cardiac and peripheral blood serum may reflect hypertension cardiac remodeling induced by AngⅡ.