Several clinical trials have demonstrated that angiotensin converting enzyme inhibitor (ACEI) and angiotensin II type I receptor blocker (ARB) are equally effective in the treatment of chronic heart failure. However, this has not been confirmed in acute cardiac dysfunction. We examined whether ACEI or ARB prevents isoproterenol induced acute left ventricular (LV) dysfunction in dogs. LV dysfunction induced by a large dose of isoproterenol (1 µg/kg/min, 3 hours infusion) was compared in dogs treated with ACEI (temocaprilat) or ARB (olmesartan) with a constant heart rate using atrial pacing and a nearly constant afterload using an adjustable aortic banding. LV systolic function (LV dP/dt, fractional shortening, ejection fraction) and diastolic function (tau, LV end-diastolic pressure) were significantly deteriorated after isoproterenol infusion. The LV dysfunction was almost totally prevented by ARB, but only partially by ACEI. The partial effect of ACEI was complemented by the co-treatment of HOE 140, a bradykinin B2 receptor antagonist. At the baseline, the dose-response to low doses of isoproterenol was significantly attenuated by ACEI, but not by ARB, and the ACEI induced attenuation was totally abolished by the co-treatment of HOE 140. The dose-response to isoproterenol was significantly attenuated after 3 hours of excess isoproterenol loading, and it was almost completely preserved by ARB, but not by ACEI. In conclusion, acute LV dysfunction and -adrenergic desensitization induced by excess isoproterenol was almost totally prevented by ARB, but only partially by ACEI. These differences were attributable, at least in part, to bradykinin pathway activated by ACEI in acute LV dysfunction.