To clarify the possible involvement of uninhibited angiotensin II (Ang II) type 2 (AT₂) receptor stimulation in the effects of an Ang II type 1 (AT₁) receptor blocker, valsartan, we examined the cardiovascular remodeling induced by aortic banding with the use of wild-type (Agtr2+) and AT₂ receptor null (Agtr2−) mice. Aortic banding caused cardiac hypertrophy in Agtr2+ and Agtr2− mice to a similar degree 6 weeks after surgery, whereas coronary arterial thickening and perivascular fibrosis were more exaggerated in Agtr2− mice. The AT₂ receptor was observed predominantly in the coronary arteries and perivascular region of Agtr2+ mice. Valsartan at a dose of 1 mg/kg per day, which did not influence systolic blood pressure, suppressed cardiac hypertrophy similarly in both strains. Valsartan inhibited coronary arterial thickening and perivascular fibrosis in both groups; however, the inhibitory effects of valsartan were significantly weaker in Agtr2− mice. The inhibitory effects of a nonselective Ang II receptor antagonist, [Sar¹,Ile⁸]-Ang II, on cardiac hypertrophy, coronary artery thickening, and perivascular fibrosis were not significantly different in Agtr2+ and Agtr2− mice. These results suggest that the improvement by valsartan of coronary arterial thickening and perivascular fibrosis after pressure overload is caused by uninhibited AT₂ receptor stimulation in addition to AT₁ receptor blockade.