2003 Fiscal Year Final Research Report Summary
Research on The Development of Overactive Bladder after Bladder Outlet Obstruction : Basic Research in Rat Model with Partial Urethral Obstruction
| Project/Area Number |
14370500
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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 | HOKKAIDO UNIVERSITY |
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Principal Investigator |
KAKIZAKI Hidehiro Hokkaido Univ., Grad School of Med., Associate Professor, 大学院・医学研究科, 助教授 (10241324)
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| Co-Investigator(Kenkyū-buntansha) |
TANAKA Hiroshi Hokkaido Univ., Grad School of Med., Instructor, 大学院・医学研究科, 助手 (60344470)
SHIBATA Takashi Hokkaido Univ., Hospital, Assistant Professor, 医学部・歯学部附属病院, 講師 (50292032)
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| Project Period (FY) |
2002 – 2003
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| Keywords | Bladder outlet obstruction / Urethral obstruction / Overactive bladder / Detrusor overactivity / Bladder afferents / Glutamate receptor / C-fiber / α1D-receptor |
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| Research Abstract |
Neuroplasticity in afferent pathways, including C-fiber afferents, is believed to be one of the major causes of overactive bladder/detrusor overactivity after bladder outlet obstruction (BOO). We examined if capsaicin sensitive C-fiber bladder afferents are involved in the development of detrusor overactivity after BOO in the rat. It is concluded that capsaicin sensitive C-fiber afferents are not essential to induce detrusor overactivity but they are involved in functional alterations in bladder afferent pathways after BOO in the rat.
Glutamate receptors have a pivotal role in the micturition reflex pathway. To determine the role of N-methyl-D-aspartate (NMDA) glutamate receptor in the development of functional bladder changes after BOO, we investigated the effects of repeat injection of MK-801, a noncompetitive NMDA receptor antagonist, on the micturition reflex in conscious obstructed rats. In obstructed MK-801 treated rats, there was a significant increase in bladder capacity and voided volume without changes in voiding efficiency or micturition pressure compared with untreated obstructed rats. The development of detrusor overactivity was not prevented by chronic treatment with IVTK-801. Thus it is concluded that BOO causes NMIDA receptor mediated alterations in bladder afferent pathways in the rat.
Detrusor overactivity in obstructed rats was suppressed by intrathecal or intrapelvic arterial injection of α1D-receptor antagonist Therefore it is concluded that spinal as well as peripheral α1D-receptors are involved in the pathophysiology of detrusor overactivity associated with BOO.
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