Aim To investigate the role of angiotensinⅡ(AngⅡ) and aldosterone (Ald) in myocardial hypertrophy and fibrosis in hypertensive rats by blocking renin angiotensin system at receptor level. Methods Thirteen 2 kidney 1 clip (2K1C) hypertensive rats began to be administered valsartan in the drinking water (10 μg/g·d) at the sixteenth week after operation. Nineteen 2K1C rats were used as untreated controls. Nineteen sham operated rats were also used as controls. 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 when three groups rats were killed at the sixteenth week, the twentieth week and the twenty eighth week after operation. Results All measured facts in 2K1C hypertensive group were significantly higher than in sham operated group (P<0.05 or 0.005). Compared with age matched 2K1C group, plasma AngⅡ concentration was higher significantly(P<0.05), but SBP, LVWI, MCC, CVF and plasma Ald concentration in treated group decreased significantly (P<0.05). Conclusions Left ventricular myocardial remodeling in renovascular hypertensive rats was closely related to myocardial AngⅡ and Ald concentration. Ang Ⅱ 1 (AT 1) receptor antagonist valsartan can block the pathophysiological effects of AngⅡ, inhibit Ald secretion and reveres left ventricular remodeling (mainly decrease deposition of type Ⅰ collagen). It suggests that AT 1 receptors may mediate the biological effects of AngⅡ in local tissue.