Ionic mechanisms of the cardiac pacemaker potential.

心脏起搏器电位的离子机制。

• 批准号: 05404017
• 负责人: NOMA Akinori
• 金额: $ 19.84万
• 依托单位: KYOTO UNIVERSITY
• 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
• 起止时间: 1993 至 1995
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-05404017/
• 关键词: 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

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.

应用膜片钳技术对兔心脏游离窦房结肌细胞进行了心脏起搏器动作电位的离子机制研究。(1)超极化激活电流由Na^+和K^+等一价阳离子携带。发现电流被Sr以时间和电压依赖的方式阻断。电流激活需要Cl^-在外部溶液中。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单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。我们发现一个新的向内电流在舒张电位范围内被激活。其药理性质与l型钙通道相似，但离子选择性不同。即电流由Na^+携带。β -肾上腺素能刺激增加了电流，这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是一致的。

项目成果

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。”

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。

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）。

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。”

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。