| Project/Area Number |
05404017
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
General physiology
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
NOMA Akinori Kyoto Univ., Physiblogy.Professor., 医学研究科, 教授 (00132738)
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| Co-Investigator(Kenkyū-buntansha) |
MITSUIE Tamotsu Kyoto Univ., Physiblogy.Associate Prof., 医学研究科, 助教授 (40174065)
尾野 恭一 九州大学, 医学部, 助手 (70185635)
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| Project Period (FY) |
1993 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥31,000,000 (Direct Cost: ¥31,000,000)
Fiscal Year 1995: ¥5,700,000 (Direct Cost: ¥5,700,000)
Fiscal Year 1994: ¥8,900,000 (Direct Cost: ¥8,900,000)
Fiscal Year 1993: ¥16,400,000 (Direct Cost: ¥16,400,000)
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| Keywords | cardiac pacemaker / sino-atrial node / Calcium ion / sustained inward current / イオンチャネル / 自動能 / 自家調節機転 |
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| Research Abstract |
The ionic mechanisms of the cardiac pacemaker action potential were studied by the patch clamp technique applied to dissociated sinoatrial node myocytes of rabbit heart. (1) The hyperpolarization-activated current was shown to be carried by monovalent cations, such as Na^+ and K^+. The current was found to be blocked by Sr in a time-and voltage-dependent manner. The current activation required Cl^- in the external solution. Varying concentrations of K^+ affected the apparent selectivity of the channels. The time-course of deactivation on depolarization was found to be dependent on the variety in the monovalent cation concentrations. A mathematical model was developed to estimate the contribution of the current to the diastolic depolarization, which was around 1-4pA.(2) We found a new inward current which is activated over the diastolic potential range. The pharmacological properties were similar to those of the L-type Ca channel, but the ion selectivity was different. Namely the current was carried by Na^+. The current was increased by the beta-adrenergic stimulation, and is consistent with the idea that this sustained inward current takes a major role in driving the diastolic depolarization.
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