Involvement of oxidative stress on detrusor overactivity

2016 Fiscal Year Final Research Report

• Project/Area Number: 26861271
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Urology
• Research Institution: Kochi University
• Principal Investigator: SHIMIZU Shogo 高知大学, 教育研究部医療学系基礎医学部門, 助教 (90721853)
• Research Collaborator: SAITO Motoaki 高知大学, 教育研究部医療学系基礎医学部門, 教授 (60273893) ; SHIMIZU Takahiro 高知大学, 教育研究部医療学系基礎医学部門, 准教授 (00363276) ; HIGASHI Youichirou 高知大学, 教育研究部医療学系基礎医学部門, 助教 (80380062) ; NAKAMURA Kumiko 高知大学, 教育研究部医療学系基礎医学部門, 技術専門職員 (30398052)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: アンジオテンシンⅡ / 排尿 / 排尿筋過活動 / 過活動膀胱 / 活性酸素

Outline of Final Research Achievements

We examined the effects of centrally administered angiotensin II (Ang II) on the micturition reflex in urethane anesthetized (1.0 g/kg, intraperitoneally) male rats. In the continuous cystometry, central administration of Ang II but not vehicle dose-dependently shortened the urinary bladder intercontraction interval, without altering the bladder detrusor pressure and blood pressure. Central administration of antagonists of Ang II type 1 (AT1) but not type 2 receptors inhibited the Ang II induced micturition reflex. These data suggest that central administration of Ang II increases urinary frequency by acting on brain AT1 receptors. Moreover, centrally administered NADPH oxidase (Nox) inhibitor apocynin changed interctonraction interval in the rat. These data suggest that central Ang II/AT1 receptor/Nox pathways are involved in the activation of micturition reflex.

Free Research Field

排尿機能学