Abstract: AIM To study the effect of telmisartan on Ang II level,AT1 R,ACE2 and MAS protein expressions in overload-induced heart failure of rats. METHODS Male Sprague Dawley rats( weighing250 g) were used to construct the pressure overload-induced heart failure model through aortic stenosis surgery. Animals were randomly divided into three groups: sham control group( n = 12),heart failure model group( HF,n = 12) and telmisartan intervention group( n = 12). Hemodynamics,heart MASs index and left ventricular MASs index,circulating and cardiac levels of angiotensin II,ACE2,AT1 R and MAS protein expressions were evaluated at week 8. RESULTS The hemodynamic meters,HMI and LVMI in HF group,improved significantly compared with those in sham control group( P < 0. 01). Levels of Ang II,AT1 R and ACE2 protein increased significantly in HF group( P < 0. 01),whereas MAS protein expressions decreased significantly compared with those in sham control group( P < 0. 01). The hemodynamic meters,HMI and LVMI in telmisartan group,were significantly lower than those in HF group( P < 0. 01). Levels of Ang II and AT1 R protein expressions were significantly lower in telmisartan group( P < 0. 01),whereas MAS and ACE2 protein expressions were significantly higher compared with those in the HF group( P < 0. 01). CONCLUSION Both downregulation of Ang II-ACE-AT1 axis and upregulation of Ang( 1-7)-ACE2-MAS axis may be involved in reversal of myocardial remodeling in heart failure by telmisartan.