| Project/Area Number |
13470331
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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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 |
OHTA Nobutaka the University of Tokyo, Faculty of Medicine, Associate professor, 医学部附属病院, 助教授 (50160510)
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| Co-Investigator(Kenkyū-buntansha) |
TAKAHASHI Satoru the University of Tokyo, Faculty of Medicine, Associate professor, 医学部附属病院, 助教授 (50197141)
TOMITA Kyoichi the University of Tokyo, Faculty of Medicine, Lecturer, 医学部附属病院, 講師 (20272578)
ARUGA Seiji the University of Tokyo, Faculty of Medicine, Assistant, 医学部附属病院, 助手 (90322057)
TSUJIMOTO Gozoh National Children's Medical Research Center, Manager/Researcher, 小児医療研究センター・小児薬理研究部, 部長(研究職)
SHINOURA Hitomi National Children's Medical Research Center, Researcher, 小児医療研究センター・小児薬理研究部, 研究員
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥14,700,000 (Direct Cost: ¥14,700,000)
Fiscal Year 2002: ¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2001: ¥11,200,000 (Direct Cost: ¥11,200,000)
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| Keywords | α1D-adrenoceptor / overactive bladder / frequency / volume analysis / α1D-knockout mice / 下部尿路通過障害 / α1D-KOマウス / 膀胱α1d受容体 / 尿道狭窄マウス / 24時間尿道モニター |
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| Research Abstract |
To study the role of α1-adrenoceptor (AR) on the urinary bladder function, we created the bladder outlet obstruction (BOO) rat model and investigated the effects of tamsulosin, an α1A/1D blocker, in this model using a frequency/volume analysis and cystometry. Furthermore, the urinary bladder function of α1D-knockout (KO) and its wild-type mice was studied. 1. The urinary frequency, bladder capacity, voided volume/micturition and bladder weight were significantly increased in the BOO group compared with the control group. 2. After tamsulosin administrations, the urinary frequency significantly decreased, and the bladder capacity and voided volume/micturition significantly increased in the both control and BOO groups. However, a more prominent change was noticed in the BOO group compared with the control group. 3. In α1D-KO mice, Voiding frequency/day was significantly lower, bladder capacity and mean volume/void was significantly larger than that in wild-type mice. No significant difference in the residual volume, maximum pressure at void and histological examinations of the bladder and urethra was observed between the two groups. These results demonstrate that although the exact sites at which α1D-AR subtype exerts its effects remain unclear, α1D-AR subtype plays an important role in regulating the bladder function.
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