Project/Area Number |
23390380
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Urology
|
Research Institution | University of Fukui |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
ITO Hideaki 福井大学, 医学部, 助教 (00345620)
TAGA Minekatsu 福井大学, 医学部附属病院, 医員 (00529349)
AKINO Hironobu 福井大学, 医学部, 准教授 (90159335)
MATSUTA Yosuke 福井大学, 医学部, 助教 (90345687)
黒川 哲之 福井大学, 医学部附属病院, 医員 (70529346)
渡邉 望 福井大学, 医学部附属病院, 医員 (80572429)
横田 義史 福井大学, 医学部, 教授 (50222386)
|
Project Period (FY) |
2011-04-01 – 2014-03-31
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥18,720,000 (Direct Cost: ¥14,400,000、Indirect Cost: ¥4,320,000)
Fiscal Year 2013: ¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2012: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2011: ¥11,310,000 (Direct Cost: ¥8,700,000、Indirect Cost: ¥2,610,000)
|
Keywords | メタボリック症候群 / 下部尿路症状 / 酸化ストレス / 膀胱虚血 / 膀胱機能 / 高血圧 / 肥満 / レニンアンギオテンシン / 食塩過剰 / プロスタグランジン |
Research Abstract |
We investigated,in rat models of metabolic syndrome (MetS) or salt-loading hypertension (HT),effects of MetS or HT on bladder function,associated changes in blood flow and epithelial mediators. These models showed frequent micturition. Amounts of ATP,PGE2 and NGF released from the stretched bladder epithelium were significantly increased. A significant decrease in blood flow was concomitant with increased oxidative stress. Angiotensin-II receptor blocker (ARB) and alpha1A blocker increased blood flow and decreased oxidative stress in the MetS bladder,resulting in suppression of detrusor overactivity. Score of lower urinary symptoms was found to be lower in male HT patients treated with ARB. Bladder ischemia and concomitant oxidative stress play an important role in development of storage dysfunction in MetS and HT via increases in release of ATP,PGE2 and NGF from the bladder epithelium. Agents increasing blood supply may improve micturition reflex via suppression of oxidative stress.
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