Investigation of mechanism of central angiotensin II-induced stimulation of micturition reflex and development of its medical treatment

2018 Fiscal Year Final Research Report

• Project/Area Number: 16K09243
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General internal medicine(including psychosomatic medicine)
• Research Institution: Kochi University
• Principal Investigator: Nakamura Kumiko 高知大学, 設備サポート戦略室, 技術専門職員 (30398052)
• Co-Investigator(Kenkyū-buntansha): 齊藤 源顕 高知大学, 教育研究部医療学系基礎医学部門, 教授 (60273893) ; 清水 孝洋 高知大学, 教育研究部医療学系基礎医学部門, 准教授 (00363276) ; 清水 翔吾 高知大学, 教育研究部医療学系基礎医学部門, 助教 (90721853)
• Project Period (FY): 2016-04-01 – 2019-03-31
• Keywords: アンジオテンシンⅡ / 排尿 / 脳 / GABA神経系 / superoxide anion

Outline of Final Research Achievements

Psychological stress leads to development of lower urinary tract dysfunctions. We previously reported that a stress related neuropeptide angiotensin II (Ang II) stimulates micturition reflex through central Ang II type 1 (AT1) receptor in rats. We investigated that the molecular mechanism which central Ang II stimulates micturition reflex in rats. The current study demonstrated that central AT1 receptor downstream signaling (phospholipase C/protein kinase C/NADPH oxidase/superoxide anion) and GABA nervous system are involved in central Ang II -induced stimulation of micturition reflex in rats.

Free Research Field

神経薬理学

Academic Significance and Societal Importance of the Research Achievements

脳内アンジオテンシンII（Ang II）タイプ1 (AT1) 受容体下流シグナル経路活性化が排尿反射亢進（頻尿）誘発に関与することが示唆された。これらシグナル因子は、ストレスのみならず他の因子に起因する頻尿の新たな治療標的になりうることが示唆された。