| Project/Area Number |
15590243
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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 |
General pharmacology
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| Research Institution | Fukuoka University |
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Principal Investigator |
KATSURAGI Takeshi Fukuoka University, School of Medicine, Professor, 医学部, 教授 (40004717)
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| Co-Investigator(Kenkyū-buntansha) |
IWAMOTO Takahiro Fukuoka University, School of Medicine, Lecturer, 医学部, 講師 (20300973)
MIGITA Keisuke Fukuoka University, School of Medicine, Research Associate, 医学部, 助手 (10352262)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2004: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2003: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | ATP release / Bradykinin / B_2-receptor / Inositol(1,4,5)tristhosthate / endoplasmic reticulum / MK-571 / MRP transporter / cultured smooth muscle cells / NEM / 培養結腸紐平滑筋細胞 / ATP放出機構 / カフェイン刺激 / 低浸透圧刺激 / Ca^<2+>シグナル / ミトコンドリア / ATP合成 |
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| Research Abstract |
Bradykinin induces the release of ATP from cultured taenia coli smooth muscle cells from guinea pigs. The evoked release was prohibited by a B2-receptor antagonist (HOE-140) and (inhibitors (U-73122 and thapsigargin) for the phospholipase C - inositol (1,4,5) P_3 signal pathway. The release of ATP was interfered, with MRP inhibitors (NM-571 and benzbromarone). However, hemichann el blockers (gap26) and the blockers (glybemclamid and Gd^<3+>) of Cl channels coupled with activation of CFTR failed to attenuate the evoked release. The release of ATP by hadykinin was also inhibited by cytochalasin D, staurosporine and NEM, but not by inhibitors for Golgi body (brefeldin A) and mitochondria (oligomycin). Therefore, we conclude that the bradykinini-evoked release of ATP may be mediated by the membrane MRP transporter activated by intracellular ATP released from endoplasmic reticulum,
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