| Project/Area Number |
23592358
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Urology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
IGAWA Yasuhiko 東京大学, 医学部附属病院, 教授 (40159588)
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| Co-Investigator(Kenkyū-buntansha) |
AIZAWA Naoki 東京大学, 医学部附属病院, 特任助教 (80595257)
HONMA Yukio 東京大学, 医学部附属病院, 教授 (40165626)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 過活動膀胱 / 間質性膀胱炎 / 求心性神経伝達 / ＴＲＰチャネル / 排尿筋低活動 / ベータ３受容体 / ムスカリン受容体 / 求心性神経活動 / 膀胱 / 加齢 / 下部尿路機能障害 / 薬物療法 |
|---|
| Research Abstract |
To find out novel therapeutic targets for bladder storage dysfunction, such as overactive bladder and hypersensitive bladder, or voiding dysfunction due to detrusor underactivity, we evaluated the mechanisms of action of antimuscarimnics, alpha1-adreonceptor (AR) antagonists, beta3-AR agonists and PDE-5 inhibitors to inhibit bladder mechanosensory afferent activities in the rat, and analyzed changes in receptors and ion channels in pathological animal models or bladder mucosa taken from patients with interstitial cystitis. The results suggest that TRPM2, A1, V4, N-type and t-type Ca2+ channels, and FAAH are promising novel targets for these bladder dysfuntions.
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