Inactivation of the E-Prostanoid 3 Receptor Attenuates the Angiotensin II Pressor Response via Decreasing Arterial Contractility

Abstract

Activation of the EP3 receptor raises baseline blood pressure and contributes to Ang II-dependent hypertension at least partially via enhancing Ca(2+) sensitivity and intracellular calcium concentration in vascular smooth muscle cells. Selective targeting of the EP3 receptor may represent a potential therapeutic target for the treatment of hypertension.