The mechanisms of regulation of nuclocytoplasmic transport of mineralocorticoid receptor by vasopressin V1a receptor.

2014 Fiscal Year Final Research Report

• Project/Area Number: 24591244
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Kidney internal medicine
• Research Institution: Kitasato University
• Principal Investigator: NONOGUCHI Hiroshi 北里大学, 北里大学メディカルセンター, 副院長 (30218341)
• Co-Investigator(Kenkyū-buntansha): NAKANISHI Takeshi 兵庫医科大学, 医学部, 教授 (70217769)
• Co-Investigator(Renkei-kenkyūsha): KAWAHARA Katsumasa 北里大学, 医学部, 教授 (70134525) ; NAKAYAMA Yushi 熊本大学, 医学部, 准教授 (00363531) ; YASUOKA Yukiko 北里大学, 医学部, 講師 (50348504) ; IZUMI Yuichiro 熊本大学, 医学部, 研究員 (20736243)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: アルドステロン / バゾプレッシン / ミネラルコルチコイド受容体 / バゾプレッシンV1a受容体 / 核内受容体 / 間在細胞 / small G protein / 酸塩基平衡

Outline of Final Research Achievements

We showed that aldosterone stimulated nucleocytoplasmic transport of mineralocorticoid receptor (MR) in rat intercalated cells using immunohistochemistry and Wester blot. Aldoterone was found to stimulate RCC-1 acticvity, whereas vasopressin decreases the activation of Ran Gap1. The presence of vasopressin V1a receptor was required for the stimulation of nucleocytoplasmic transpoort of MR.
Aldosterone and vasopressin stimulate PKC pathway. However, aldosterone stimulates atyoical or novel PKC pathways whereas vasopressin stimulate conventional PKC pathway. Although EGF receotor has been thought to be a membrane-bound receptor of aldosterone, further investigations are required to draw the conclusion.

Free Research Field

腎生理