Aim To investigate the role of angiotensin Ⅱ(AngⅡ) 1 type recepter antagonist and aldosterone (Ald) receptor antagonist in reversing myocardial remodeling in hypertensive rats by blocking renin angiotensin system at receptor level and the mechanism of hypertensive myocordial remodeling. Methods Thirty nine male Wistar rats were devided into the shamo operated group, the hypertension group, the valsartan group [10 μg/(kg·d)] and spironolactone group [40 mg/(kg·d)]. Systolic blood pressure (SBP), left ventricular weight index (LVWI), plasma and myocardial AngⅡ/Ald concentration, myocardial collagen concentration (MCC) and collagen volume fraction (CVF) were measured at the sixteenth week, the twentieth week and the twenty eighth week after operation. The pathologic characterization of myocardial Ⅰ type and Ⅲ type collagen was observed at the same time. Results All measured datas in 2K1C hypertension group were significantly higher than in shamo operated group (p<0.05 or 0.005). Compared with hypertension group, plasma AngⅡ concentration was significantly higher (p<0.05), but SBP, LVWI, MCC mainly Ⅰ type collagen, CVF and plasma Ald concentration in the valsartan group decreased significantly (p<0.05). Treatment with spironolactone lightly decreased SBP, LVWI, MCC and CVF in early, but significantly lowered LVWI, MCC and CVF (p<0.05), especially Ⅲ type collagen. Conclusions It indicated that development of the LVH and myocardial fibrosis is heterochronia. This study suggested AngⅡ and aldsterone play a vital role in hypertensive myocardial remodeling. AT 1 receptor mainly mediats type I collagen deposition while aldosterone receptor mainly mediates type Ⅲ collagen deposition.