2013 Fiscal Year Final Research Report

Analysis of a novel mechanism responsible for postmenopausal hypertension

Research Project

Project/Area Number	23590296
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	General pharmacology
Research Institution	Chiba University
Principal Investigator	KIMURA Sadao 千葉大学, 医学(系)研究科(研究院), 教授 (40134225)
Co-Investigator(Kenkyū-buntansha)	NISHIYAMA Mariko 千葉大学, 大学院医学研究院, 助教 (00092081) USUI Hirokazu 千葉大学, 大学院医学研究院, 講師 (90375634)
Project Period (FY)	2011 – 2013
Keywords	閉経後高血圧 / アンジオテンシン / アンジオテンシン受容体 / RGS / スピノフィリン
Research Abstract	This study showed that (1) RGS2 and spinophilin (SPL) are present in vascular smooth muscle cells, (2) RGS2 showed potent inhibitory effects on intracellular calcium responses induced by Ang II in HEK293T cells stably expressing AT1 receptors, (3) SPL strongly enhanced the inhibitory effects of RGS2 on AT1 receptor calcium signaling, and (4) estrogen increased the expression of SPL in vascular smooth muscle cells. These results strongly suggests that loss of circulating estrogen in blood decreases the expression of SPL in smooth muscle cells, and the decreased expression of SPL weakens the inhibitory effects of RGS2 enhanced by SPL, leading to the development of hypertension in postmenopausal women.

(5 results)