| Project/Area Number |
04670055
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
General physiology
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| Research Institution | The Jikei University School of Medicine |
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Principal Investigator |
KURIHARA Satoshi Faculty of Medicine, Physiology, Prof., 医学部, 教授 (90057026)
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| Co-Investigator(Kenkyū-buntansha) |
TANAKA Etsuko Faculty of Medicine, Physiology, Research Associate, 医学部, 助手 (70256410)
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1993: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1992: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | Intracellular Ca / Cardiac muscle / Temperature / Sarcoplasmic reticulum / Na-Ca exchange / Mitochondria / Na‐Ca交換系 / カフェイン / リアノジン / 急速冷却 |
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| Research Abstract |
The release of Ca from the SR is triggered by an influx of Ca as Ca current, which is called Ca-induced Ca release (CICR). On the other hand, rapid lowering the temperatrure of the bathing solution releases Ca from the SR, which is called rapid cooling Ca release (RCCR). We investigated the mechanism of RCCR in ferret ventricular muscles using aequorin. Rapid cooling from 30^0 to below 4^0 transiently increased intracellular Ca concentration without accompanying action potential. RCCR was not influenced by changing K concentration in the solution. RCCR was not observed in the ryanodine-treated preparations. Therefore, the source of Ca in rapid cooling is the SR and RCCR is not due to a membrane depolarization. The amount of Ca released by rapid cooling was not influenced by the Ca concentration just before the rapid cooling. RCCR was inhibited in Na-free solutions (Li and TMA replacement) but the application of caffeine just after the RCCR in Na-free solutions released more Ca than that in the RCCR.The result suggests that the mechanism of RCCR is different from that of caffeine-induced Ca release. The decay of Ca singal at 4^0C was slightly inhibited by the inhibitors of Na-Ca exchanger and the Ca pump of the SR.However, ruthenium red markedly inhibited the decay of Ca signal. Therefore, sufficient Ca might be transported by mitochondria at 4^0C.These results suggest that rapid cooling releases Ca from SR without a significant membrane potential change and is an useful method to assess the accumulated Ca in SR.
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