| Project/Area Number |
14570040
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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 | KYOTO UNIVERSITY |
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Principal Investigator |
MITSUIYE Tamotsu Kyoto University, Physiology, Associate Professor, 医学研究科, 助教授 (40174065)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2002: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | cold stress / cardiac myocytes / G-protein / L-type Ca channels / autonomic regulation / heart rate variability / カルシウムチャネル / 心拍数 / 自律神経 / 呼吸 / 寒冷適応 / 心ペースメーカー細胞 / G蛋白 / 膜電流 |
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| Research Abstract |
Mice were bred in a cold room (15 ℃), and the effects of the cold stress on the L-type Ca channel of cardiac ventricular and pacemaker cells were analyzed. The G-protein dependent slow inactivation kinetics of the L-type Ca channels developed within a week. The slow inactivation in cold acclimated mice was abolished by dialyzing cell with GDP-γS through pipette. However, the slow inactivation was not observed in cells dissociated from mice bred in a warm room (30 ℃) even after the dialysis with GTP-γS These results suggested that small G-proteins may be involved in the slow inactivation. Mice model is profitable for the analysis of the long-term regulation of ionic channels, which is caused by cold stress because the acclimation occurs within a week. Analysis of the autonomic activities by measuring RR-intervals revealed that the rapid cold exposure of mice not only increase the heart rate but also suppress the variation of the beat to beat intervals. Thus it may be suggested that the heart of the cold stressed mice are always exposed to the mechanical stress attributable to the thoracic pressure change by ventilations. To further study the relationship between the respiration and heart rate, I developed a new system for recording and analyzing autonomic regulation of the heart.
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