| Project/Area Number |
18590789
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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 |
Circulatory organs internal medicine
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| Research Institution | Jikei University School of Medicine |
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Principal Investigator |
KOMUKAI Kimiaki Jikei University School of Medicine, 医学部, 講師 (60360145)
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| Co-Investigator(Kenkyū-buntansha) |
HONGO Kenichi 東京慈恵会医科大学, 医学部, 准教授 (00256447)
KAWAI Makoto 東京慈恵会医科大学, 医学部, 講師 (40277025)
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| Project Period (FY) |
2006 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥3,110,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥510,000)
Fiscal Year 2009: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2008: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2007: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2006: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | エンドセリン / カルシウム電流 / 心筋 / シグナル伝達 / CaMKII / プロテインキナーゼC / パッチクランプ法 / ETA受容体 / プロテインキナーゼ / ラット / カルシウム / ETB受容体 / 生理活性 / α受容体 / アンギオテンシン / KN-93 |
|---|
| Research Abstract |
We investigated the effect of endothelin-1 (ET-1) on L-type Ca current (ICa) of rat ventricular myocytes using perforated patch clamp technique. ET-1 (10nM) increased ICa. This increase was blocked by a selective ETA antagonist BQ-123 but not by a selective ETB antagonist BQ-788. The increase was blocked by a PKC inhibitor chelerythrine and a CaMKII inhibitor KN-93 but not by its inactive analogue KN-92. The increase was blocked by another CaMKII inhibitor AIP. These results suggested that ET-1 increased ICa via an ETA-PKC-CaMKII pathway.
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