| Project/Area Number |
26670705
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Urology
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| Research Institution | Nagoya City University |
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Principal Investigator |
HASHITANI HIkaru 名古屋市立大学, 大学院医学研究科, 教授 (10315905)
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| Co-Investigator(Kenkyū-buntansha) |
西川 信之 名古屋市立大学, 大学院医学研究科, 研究員 (30722748)
三井 烈 名古屋市立大学, 大学院医学研究科, 講師 (90434092)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 低活動膀胱 / 平滑筋 / 粘膜筋板 / 副甲状腺ホルモン関連ペプチド / TRPV4チャネル / 血小板由来成長因子α受容体 / SK３チャネル / 副甲状腺ホルモン関連蛋白 / カルシウム活性化カリウムチャネル / PDGFRα陽性間質細胞 / 小コンダクタンスカルシウム活性化カリウムチャネル / 排尿筋平滑筋 / 膀胱粘膜筋板 / 活動電位 / ぺリサイト |
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| Outline of Final Research Achievements |
Role of intrinsic relaxation mechanisms of the bladder in regulating spontaneous contractility was investigated in smooth muscles of detrusor and muscularis mucosae. PTHrP, an endogenous muscle relaxant released from detrusor upon bladder wall distension, had a more pronounced inhibitory effects on spontaneous contractions of detrusor than those of muscularis mucosae. TRPV4, a Ca2+-permeable stretch-activated cation channels expressed in both detrusor and muscularis mucosae. Ca2+ influx through TRPV4 appears to activate BK channels to suppress spontaneous contractions, and thus a functional coupling of TRPV4 with BK channels may act as a self-limiting mechanism for bladder contractility. SK channel openers prolonged the after-hyperpolarization in both detrusor and muscularis mucosae, indicating the SK channels expression in not only PDGFRα (+) cells but also detrusor. Upregulation of these intrinsic relaxation mechanisms may result in underactive bladder.
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