Ionic mechanisms of the cardiac pacemaker potential.
Ionic mechanisms of the cardiac pacemaker potential.
批准号:
05404017
负责人:
NOMA Akinori
金额:
$19.84万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for General Scientific Research (A)
财政年份:
1993
资助国家:
日本
项目状态:
已结题
起止时间:
1993 至 1995
中文摘要
将膜片钳技术应用于分离的兔心窦房结细胞,研究了心脏起搏器动作电位的离子机制。(1)超极化激活电流主要由Na~(++)、K~(++)等一价阳离子携带。电流被锶以时间和电压依赖的方式阻断。当前的激活需要外部溶液中的Cl^-。不同浓度的K~(++)影响通道的表观选择性。发现去极化失活的时间过程依赖于一价阳离子浓度的变化。建立了一个数学模型来估计电流对舒张期去极化的贡献,约为1-4pA。(2)我们发现了一种新的内向电流,它在舒张期电位范围内被激活。其药理性质与L钙通道相似,但离子选择性不同。也就是说,电流由Na~(++)携带。该电流被β-肾上腺素能刺激所增加,并与这种持续的内向电流在驱动舒张期去极化中起主要作用的观点一致。
英文摘要
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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Ono, K.: "Voltage-and time-depondent block of I_f by Sr^<2+> in rabbit sino-atriel node cells." Pfliigens Archiv. 427. 437-443 (1994)
Ono, K.:“在兔窦房结细胞中,Sr^<2> 对 I_f 的电压和时间依赖性阻断。”
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通讯作者:
Ito, H.: "Arapidl activating dlayed rectifie K^+ channel in rabbit Isinoctial node cells" American Journal of Physiology. 269. H443-452 (1995)
Ito, H.:“Arapidl 激活兔等交节细胞中的延迟整流 K^ 通道”美国生理学杂志。
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Maruoka F.: "Cation-dependent gating of the hyperpolarization-activaleil cation current in roffit sino-atcial node cells." Journal of Physiology. (発表予定). (1994)
Maruoka F.:“roffit 窦房结细胞中超极化激活阳离子电流的阳离子依赖性门控。”生理学杂志(1994 年)。
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Ito H., Ono K., and Noma A.: "Background conductance attributable to spontaneous opening of muscarinic K^+ channels in rabbit sino-atrial node cells." Journal of Physiology. 476.1. 55-68 (1994)
Ito H.、Ono K. 和 Noma A.:“背景电导归因于兔窦房结细胞中毒蕈碱 K^ 通道的自发开放。”
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Masuoka, F: "Cation-dependent gating of the by Pyalaing alcon-activalid cation current" Journal of Physiology. 477. 423-435 (1994)
Masuoka, F:“Pyalaing alcon-activalid 阳离子电流的阳离子依赖性门控”生理学杂志。
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共 23 条
Mechanisms underlying cell function of cardiac myocytes and pancreatic・cells by developing mathematical cell models
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A novel sustained inward current activated at the diastolic pacemaker potential
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