| Project/Area Number |
14570051
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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 physiology
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| Research Institution | Fukuoka University |
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Principal Investigator |
UEHARA Akira Fukuoka University, School of Medicine, Associate Professor, 医学部, 助教授 (60140745)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
|
| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2003: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2002: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | Heart / Calcium / Sarcoplasmic reticulum |
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| Research Abstract |
We have explored whether the capacitative Ca^<2+> entry (CCE) mechanisms exists in heart muscle with a fluorescent [Ca]_i measurement technique. By the reintroduction of external Ca^<2+> after the depletion of Ca^<2+> stored in sarcoplasmic reticulum (SR) using Ca^<2+> pump inhibitors or ryanodine receptor (RyR) activators, a huge steady rise in cytoplasmic Ca^<2+> concentration at both tissue and single cell levels was evoked even in the presence of L-type Ca^<2+> channel antagonists. Such a CCE activity was sensitive to Zinc but insensitive to the other many cation blockers in possible molecular entities of CCE channels of TRP and Icrac channel families. Here we could thus first demonstrate from embryonic to neonatal stages at least that the PL membrane of the cardiac myocyte is endowed with a store-operated Ca^<2+> entry pathway. Cardiac SR could be refilled with Ca^<2+> via the CCE pathway and reset as a functional regulator of the cytoplasmic Ca^<2+> concentration to induce the multiple Ca^<2+> dependent cellular function, whenever the stored Ca^<2+> in the SR lumen is consumed and subsequently depleted during ontogenetic developing stages or under some physiological and pathophysiological conditions.
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