| Project/Area Number |
09470010
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Sapporo Medical University |
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Principal Investigator |
TOHSE Noritsugu School of Medicine, Sapporo Medical University Professor, 医学部, 教授 (80192657)
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| Co-Investigator(Kenkyū-buntansha) |
NAGASHIMA Masato School of Medicine, Sapporo Medical University Assistant Professor, 医学部, 講師 (20264525)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥13,400,000 (Direct Cost: ¥13,400,000)
Fiscal Year 1998: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1997: ¥11,300,000 (Direct Cost: ¥11,300,000)
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| Keywords | ion channel / cloning / cardiomyocyte / patch clamp / PCR method / Development / K channel |
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| Research Abstract |
In an analysis of fetal rat ventricular myocytes using the patch clamp method, resting membrane potential of the cardiomyocytes shifted to hyperpolarization. The hyperpolarization during the fetal period abolished automaticity observed in middle fetal period, and kept resting membrane potential stable. In whole-cell voltage clamp, the inward rectifier KィイD1+ィエD1 current (IK1) gradually increased during the developmental period, and then was 12-folds comparing that in the middle fetal period. Therefore,the hyperpolarization may be produced by the increase in IK1. Mechanisms of the increase in IK1 was understood not to be simple when single channel recording was performed. During the developmental period, it was not observed that one type of channel showed an increase in the number of channels or in open probability. In the late fetal period, channels possessing larger unit conductance than that in the middle fetal period opened frequently. In analysis of gene coding IK1 channels(Kir 2 family), Kir 2.1 and Kir 2.2 were expressed in rat fetal cardiomyocytes. The quantitative PCR method showed that expression of Kir2.2 increased in 17-folds in spite of only 2-folds increase in Kir 2.1 from the middle to the later fetal period. Therefore, these data suggest that IK1 channel coded by Kir2.2 becomes predominant during fetal development, and then produces hyperpolarization of ventricular cardiomyocytes.
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