| Project/Area Number |
13672274
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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 |
Biological pharmacy
|
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| Research Institution | The University of Tokyo |
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Principal Investigator |
AKAHANE Satomi The University of Tokyo, Graduate School of Pharmaceutical Sciences, Research Associate, 大学院・薬学系研究科, 助手 (00184185)
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|---|
| Project Period (FY) |
2001 – 2003
|
| Project Status |
Completed (Fiscal Year 2003)
|
| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥1,300,000 (Direct Cost: ¥1,300,000)
|
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| Keywords | calcium channel / calcium / calcium antagonist / dihyrdropyridines / Ca^<2+>チャネル / ゲーティング |
|---|
| Research Abstract |
The voltage-dependent L-type Ca^<2+> channel plays a key role in the spatial and temporal regulation of Ca^<2+>. In cardiac excitation-contraction coupling, Ca2 tinduced Ca^<2+> release (CICR) from ryanodine receptors (RyRs), triggered by Ca^<2+> entry through the nearby L-type Ca^<2+> channel, induces the Ca^<2+>-dependent inactivation (CDI) of the Ca2ア channel. We demonstrated that the CICR-dependent CDI of L-type Ca^<2+> channels, under control of the privileged cross-signaling between L-type Ca^<2+> channels and RyRs, plays important roles for monitoring and tuning the SR Ca^<2+> content via changes of AP waveform and the amount of Ca^<2+>-influx during AP in ventricular myocytes.
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