Calcim Independent Contraction Of Human Bladder Smooth Muscle
Project/Area Number |
06671603
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
Urology
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Research Institution | FUKUSHIMA MEDICAL COLLEGE |
Principal Investigator |
YOSHIMURA Yasukuni Fukushima Medical College, Dept.of Ulology, Instructor, 医学部, 講師 (50220744)
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Co-Investigator(Kenkyū-buntansha) |
YAMANAKA Naoto Fukushima Medical College, Dept.of Ulology, 医学部, 助手 (80254035)
SUZUKI Takayuki Fukushima Medical College, Dept.of Ulology, Associate Professor, 医学部, 講師 (40192132)
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Project Period (FY) |
1994 – 1995
|
Project Status |
Completed (Fiscal Year 1995)
|
Budget Amount *help |
¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1995: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1994: ¥1,000,000 (Direct Cost: ¥1,000,000)
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Keywords | calcium independent contraction / bladder smooth muscle / protein kinase C / calcium ion / stored calcium / 細胞内カルシウム濃度 / 細胞内情報伝達機構 / プロテインキナーゼ阻害剤 |
Research Abstract |
Background : Recently, it has been suggested in vascular smooth muscle that a Ca^<2+>-independent mechanism or Ca^<2+>-sensitization of contractile elements may participate in smooth muscle contraction. In this study, we evaluate this mechanism in detrusor muscle. Methods : Strips from rabbit aorta, rabbit bladder and human bladder were evaluated by in vitro contraction studies. Results : The results show that 1) in Ca^<2+>-free solution containing EGTA,carbachol (Cch) and phorbol ester produce sustained contractions in detrusor muscle (Ca^<2+>-free contraction) ; 2) depletion of Ca^<2+> stores by caffeine does not affect Ca^<2+>-free contraction induced by Cch ; 3) W-7 (CaM inhibitor) and ML-9 (MLCK inhibitor) do not show inhibitory effects on Ca^<2+>-free contraction, while H-7 (PKC inhibitor) abolishes this contraction. Conclusions : These results suggest that neither stored Ca^<2+> nor Ca^<2+>-CaM-MLCK system is not involved in the Cch-induced Ca^<2+>-free contraction of detrusor muscle. This Ca^<2+>-independent contraction seems to be mediated by the activation of PKC coupled with receptor agonist stimulation.
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Report
(3 results)
Research Products
(4 results)