A study on the molecular basis of the cardiac inward rectifier potassium channels

心脏内向整流钾通道的分子基础研究

基本信息

  • 批准号:
    15590187
  • 负责人:
  • 金额:
    $ 2.24万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    2003
  • 资助国家:
    日本
  • 起止时间:
    2003 至 2004
  • 项目状态:
    已结题

项目摘要

1.The amplitude of the currents through the cardiac strong inward rectifier potassium (K^+) channels is known to be regulated by a voltage-dependent blockade of the channels by intracellular polyamines and Mg^<2+>. However, the detailed mechanism of the blockade is complicated, and is not well understood. We expressed Kir2.1,which is the major subunit of the cardiac inward rectifier K^+ channels, in human embryonic kidney cells 293T and studied the polyamine and Mg^<2+> blockades of the Kir2.1 channel currents recorded from inside-out patch membranes using the voltage-clamp method. We found that the Kir2.1 currents recorded in the presence of various concentrations of cytoplasmic polyamines and Mg^<2+> can be all well described as those flowing through two populations of Kir2.1 channels having different sensitivities to the blockades by polyamines and Mg^<2+>. The relative size of the two populations was slightly altered by an interaction of polyamines with the channel at an intracellu … More lar regulatory site. Our results suggested that the outward currents through the cardiac inward rectifier K^+ channels flow mostly through a small population (〜10%) of the channels having lower sensitivity to cytoplasmic blockers. Physiological concentrations of intracellular Mg^<2+> blocks a major population (〜90%) of the channels showing higher sensitivity to cytoplasmic blockers and thereby increases the amplitude of the outward currents in the presence of polyamines.2.We studied the mechanisms underlying the difference between the strong inward rectifier K^+ currents in the cardiac atrial and ventricular myocytes. Our results indicated that the difference in the subunits (Kir2.1,Kir2.2,or Kir2.3) composing the channel cannot explain the difference, but a higher concentration of intracellular polyamines can change the currents flowing through the Kir2.1 channels from a ‘ventricular type' to an ‘atrial type'. The total and free polyamine concentrations measured were indeed higher in the atrial tissues of the guinea-pig hearts. Less
1.已知通过心脏强内向整流钾(K^+)通道的电流幅度受细胞内多胺和镁离子的电压依赖性阻断。然而,封锁的详细机制是复杂的,而且还没有被很好地理解。我们在人胚胎肾细胞293T中表达了心脏内向整流钾通道的主要亚基Kir2.1,并用电压钳方法研究了多胺和镁离子对由内向外膜记录的Kir2.1通道电流的阻断作用。我们发现,在不同浓度的胞质多胺和镁离子存在下记录到的Kir2.1电流都可以很好地描述为流经两组Kir2.1通道的电流,这两组通道对多胺和镁离子的阻断具有不同的敏感性。这两个群体的相对大小由于多胺与细胞内…通道的相互作用而略有改变更大的监管网站。我们的结果表明,流经心脏内向整流钾通道的外向电流主要流经对胞浆阻滞剂敏感性较低的通道中的一小部分(~10%)。生理浓度的细胞内镁离子阻断了大多数(~90%)对胞浆阻滞剂敏感的通道,从而在多胺存在下增加了外向电流的幅度。2.我们研究了心脏心房和心室肌细胞强内向整流钾电流差异的机制。我们的结果表明,构成通道的亚基(Kir2.1、Kir2.2或Kir2.3)的差异不能解释这种差异,但细胞内较高浓度的多胺可以将流经Kir2.1通道的电流从“室型”改变为“房型”。在豚鼠心脏的心房组织中,测得的总多胺和游离多胺浓度确实较高。较少

项目成果

期刊论文数量(24)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Different intracellular polyamine concentrations underlie the difference in the inward rectifier K+ currents in atria and ventricles of the guinea‐pig heart
  • DOI:
    10.1113/jphysiol.2004.077677
  • 发表时间:
    2005-03
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Ding-Hong Yan;K. Nishimura;Kaori Yoshida;K. Nakahira;T. Ehara;K. Igarashi;K. Ishihara
  • 通讯作者:
    Ding-Hong Yan;K. Nishimura;Kaori Yoshida;K. Nakahira;T. Ehara;K. Igarashi;K. Ishihara
Cell-volume regulation by swelling-activated chloride current in guinea-pig ventricular myocytes.
豚鼠心室肌​​细胞中肿胀激活的氯电流调节细胞体积。
  • DOI:
  • 发表时间:
    2004
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Yan D-H;Ishihara K.;Yan D-H;Yan D-H;Ishihara K;Yamamoto S
  • 通讯作者:
    Yamamoto S
Ishihara, K: "Two modes of polyamine block regulating the cardiac inward rectifier K^+ Current I_<K1> as revealed by a study of the Kir2.1 channel expressed in a human cell line"Journal of Physiology ; DOI : 10.1113/jphysiol.2003.055434. (2004)
Ishihara, K:“对人类细胞系中表达的 Kir2.1 通道的研究揭示了调节心脏内向整流器 K^ 电流 I_<K1> 的两种多胺阻断模式”生理学杂志;
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Two modes of polyamine block regulating the cardiac inward rectifier K+ current IK1 as revealed by a study of the Kir2.1 channel expressed in a human cell line
  • DOI:
    10.1113/jphysiol.2003.055434
  • 发表时间:
    2004-04-01
  • 期刊:
  • 影响因子:
    5.5
  • 作者:
    Ishihara, K;Ehara, T
  • 通讯作者:
    Ehara, T
Two Kir2.1 channel populations with different sensitivities to Mg2+ and polyamine block: a model for the cardiac strong inward rectifier K+ channel
  • DOI:
    10.1113/jphysiol.2004.079186
  • 发表时间:
    2005-03
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Ding-Hong Yan;K. Ishihara
  • 通讯作者:
    Ding-Hong Yan;K. Ishihara
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YANAGI Keiko其他文献

YANAGI Keiko的其他文献

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{{ truncateString('YANAGI Keiko', 18)}}的其他基金

Molecular mechanisms of the physiologically relevant component of the inward rectifier potassium channels that shows low sensitivity to the channel blockers
对通道阻滞剂表现出低敏感性的内向整流钾通道生理相关成分的分子机制
  • 批准号:
    22590208
  • 财政年份:
    2010
  • 资助金额:
    $ 2.24万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Elucidation of the molecular mechanisms of the inward rectifier potassium channel function using electrophysiological and optical approaches
使用电生理学和光学方法阐明内向整流钾通道功能的分子机制
  • 批准号:
    19590209
  • 财政年份:
    2007
  • 资助金额:
    $ 2.24万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
A study on the regulation of the inward rectifier potassium current by polyamine.
多胺调节内向整流钾电流的研究
  • 批准号:
    17590188
  • 财政年份:
    2005
  • 资助金额:
    $ 2.24万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)

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肌间丛表达的离子通道型孤儿受体的功能分析。
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