Upregulation of Angitensin II Type I Receptor and Connexin 43 in the Bladder of Aged Rats with Bladder Dysfunction

2015 Fiscal Year Final Research Report

• Project/Area Number: 25462515
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Urology
• Research Institution: Oita University
• Principal Investigator: MORI Kenichi 大分大学, 医学部, 助教 (00579013)
• Co-Investigator(Kenkyū-buntansha): Mimata HIROMITSU 大分大学, 医学部, 教授 (60219714) ; Sumino YASUHIRO 大分大学, 医学部, 講師 (30325716)
• Research Collaborator: Yoshimura NAOKI 米国ピッツバーグ大学, 泌尿器科, 教授
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 加齢 / 排尿機能障害 / レニン-アンジオテンシン系 / AT1受容体 / AT2受容体 / コネキシン43

Outline of Final Research Achievements

We examined alterations in expression of angiotensin II type 1 receptors (AT1R) which induce organ tissue remodeling, angiotensin II type 2 receptors (AT2R) which protect against it, and related molecules in the bladder of matured rats with bladder dysfunction. In the bladder, the mRNA expression of AT1R, Cx43, MAPK, collagen 1, and AT2R were significantly higher in mutured rats than young rats. The relative expression ratio of AT1R protein against AT2R protein in the mucosa and detrusor was significantly increased in mutured versus young rats. Matured rats exhibit not only bladder overactivity but also impaired voiding, which are associated with upregulation of AT1R. The upregulation of AT2R also may play a significant role in the suppressing of AT1R induced remodelling. However, because AT1R upregulation is more dominant than AT2R increases, AT2R activation may not be sufficient to suppress AT1R stimulation in matured rats.

Free Research Field

排尿機能学