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AT₂ receptors contribute to acute blood pressure-lowering and vasodilator effects of AT₁ receptor antagonism in conscious normotensive but not hypertensive rats

Departments of ¹Physiology and ²Pharmacology, Monash University, Victoria, Australia

Submitted 27 October 2004 ; accepted in final form 20 December 2004

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) rats, and sham-operated 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 AT₂ receptor activation. Heart rate, mean arterial pressure, and regional hemodynamics were measured over a 4-day protocol in rats that received the following treatments in randomized order: saline vehicle, the AT₁ receptor antagonist candesartan (0.1 mg/kg iv bolus), the AT₂ receptor antagonist PD-123319 (50 µg·kg^–1·min^–1), 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 PD-123319 significantly affected these variables. Concomitant PD-123319 administration partially reversed the depressor and mesenteric vasodilator effects of candesartan in sham-operated normotensive rats but not in SHR or 2K1C 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.

angiotensin receptors; candesartan; PD-123319; regional hemodynamics; hypertension; renal

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