The aims of this study were to determine the contribution of the AT₂-receptor to the antihypertensive and regional vasodilatory effects of AT₁-receptor blockade in adult spontaneously hypertensive rats (SHR), 2 kidney, 1 clip hypertensive (2K1C) and shamoperated normotensive rats. Several studies have provided evidence to support the notion that the AT₂-receptor may have opposing effects to those mediated by the AT₁-receptor. We therefore tested the hypothesis that the depressor and vasodilator effects of acute AT₁-receptor blockade are dependent on AT₂receptor activation. Heart rate, mean arterial pressure and regional hemodynamics were measured over a 4-day protocol in rats that received the following treatments in randomised order: saline vehicle, the AT₁-receptor antagonist candesartan (0.1 mg/kg i.v bolus), the AT₂- receptor antagonist PD123319 (50 µg/kg/min), or both antagonists. Intravenous candesartan reduced mean arterial pressure in all groups of rats, and this was accompanied by renal and mesenteric vasodilation. Neither saline nor PD123319 significantly affected these variables. Concomitant PD123319 administration partially reversed the depressor and mesenteric vasodilator effects of candesartan in sham-operated normotensive rats, but not in SHR or 2K1C hypertensive rats. These data indicate that the AT₂-receptor contributes to the blood pressure-lowering and mesenteric vasodilator effects of AT₁-receptor blockade, in the acute setting in conscious normotensive, but not hypertensive, rats.