Arterial Smooth Muscle Cell PAQR7 Activation Attenuates Myogenic Tone In Pressurized Cerebral Arteries

Abstract

Sex steroid hormones (estrogen, progesterone) are regulators of arterial contractility. Specifically, progesterone exerts rapid, nongenomic vasodilation via membrane receptors termed membrane progesterone receptors (mPR) belonging to the GPCR-like family of Progestin & Adiponectin Q Receptors (PAQR). Moreover, PAQR7 (mPRα) is reportedly expressed in smooth muscle cells (SMC) of human conduit vessels and has a putative role in vasodilation. However, the expression and function of PAQR7 in pressurized resistance size arteries, arteries that regulate local blood flow and blood pressure, have not been investigated. PURPOSE: To examine the expression and physiological function of PAQR7 in cerebral resistance size arteries. METHODS: RT-PCR was performed on whole cerebral arteries and isolated arterial SMCs to detect PAQR7 mRNA expression. Western blotting was performed on whole cerebral arteries to examine PAQR7 protein expression. Pressurized artery myography was performed on endothelium-intact and -denuded cerebral arteries to examine the role of SMC PAQR7 in vasodilation using the PAQR7-specific agonist, Org OD 02-0. RESULTS: PAQR7 mRNA (whole artery and isolated arterial SMCs) and protein were detected in resistance size cerebral arteries (n=4). Interestingly, there were no significant differences in vasodilation between endothelium-intact and -denuded arteries at any concentration (10-9M to 10-5M, n=4). CONCLUSION: These data suggest that arterial smooth muscle PAQR7 activation elicits vasodilation in pressurized resistance size arteries.