| Project/Area Number |
12671543
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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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 | Kyushu University |
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Principal Investigator |
SEKI Narihito Department of Urology, Assistant professor, 医学部附属病院, 講師 (90294941)
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| Co-Investigator(Kenkyū-buntansha) |
TERAMOTO Noriyoshi Department of Pharmacology, Assistant professor, 大学院・医学研究院, 講師 (40294912)
ITO Yushi Department of Pharmacology, Professor, 大学院・医学研究院, 教授 (80037506)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2000: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | human detrusor / ATP / Purinergic receptor / Potassium channel / neuro-muscular transmission / Acetylcholine / Patch clamp / スルフォニルウレア受容体 / ヒト膀胱排尿筋 / 細胞内微小電極法 / 脱分極 |
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| Research Abstract |
Patch-clamp experiments were performed using dispersed human detrusor myosites. In conventional whole-cell configuration (symmetrical 140 mM K^+ conditions, 500 μM ATP in pipette solution), application of 100 μM pinacidil caused an inward K^+ current that was suppressed by 5 μM glibenclamide at a holding potential of -60 mV. In cell-attached configuration, K_<ATP> channels (approximately 4.8 pA, 80 pS) were activated by 100 μM pinacidil and were reveresibly suppressed by 1 μM glibenclamide at -60 mV. The activity of K_<ATP> channels was readily observed just after the establishment of inside-out configuration, and channel activity was suppressed by internal application of 100 μM ATP. These electrophysiological properties are similar to those of native and recombinant K_<ATP> channels which are composed of Kir6.2. These results suggest that the pore region protein of human detrusor K_<ATP> channels is likely to be Kir6.2.
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