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Properties and role of the delayed rectifier K^+ current in the pacemaker activity

Research Project

Project/Area Number 11670040
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field General physiology
Research InstitutionShiga University of Medical Science

Principal Investigator

MATSUURA Hiroshi  Shiga University of Medical Science, Physiology, Professor, 医学部, 教授 (60238962)

Co-Investigator(Kenkyū-buntansha) DING Wei-guang  Shiga University of Medical Science, Physiology, Research Associate, 医学部, 助手 (80242973)
OMATSU-KANGE Mariko  Shiga University of Medical Science, Physiology, Associate Professor, 医学部, 助教授 (80161397)
Project Period (FY) 1999 – 2000
Project Status Completed (Fiscal Year 2000)
Budget Amount *help
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2000: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1999: ¥2,000,000 (Direct Cost: ¥2,000,000)
Keywordssino-atrial node / pacemaker activity / delayed rectifier K^+ current / I_<Kr> / I_<Ks> / maximum diastolic potential / envelope of tails test / E-4031 / 心臓自動能 / P2Y受容体 / サイクリックGMP / サイクリックGMP依存性蛋白キナーゼ
Research Abstract

The present research project was undertaken to investigate the properties and role of the delayed rectifier K^+ current (I_K) in isolated guinea-pig sino-atrial (SA) node pacemaker cells using the whole-cell configuration of the patchclamp technique. An envelope of tails test conducted in the absence and presence of a potent methanesulfonanilide I_<Kr> blocker E-4031 (5 μM) indicated that I_K comprises the drug-sensitive, rapidly activating and drug-resistant, slowly activating components of I_K (I_<Kr> and I_<Ks>, respectively) in guinea-pig SA node cells. The activation range for I_<Ks>, defined as the E-4031-sensitive current (half-activation voltage, V_<1/2>, of -26.2 mV) was much more negative than that for I_<Ks>, defined as the E-4031-resistant current (V_<1/2> of +17.2 mV). I_<Kr> exhibited a marked inward rectification at potentials positive to -50 mV, whereas I_<Ks> showed only a slight rectification. The tail current amplitude of I_<Kr> was comparable to that of I_<Ks>, when … More measured upon repolarization to -50 mV after a 100-ms depolarizing pulse to +20 mV, simulating an action potential. In the current-clamp experiment, a bath application of E-4031 (0.5 and 5 μM) initially delayed the repolarization phase at potentials negative to approximately -30 mV without producing any appreciable effect on repolarization at more depolarized potentials and depolarized the maximum diastolic potential in spontaneous action potentials. These results strongly indicate that the late phase of repolarization (at potentials negative to -30 mV) leading to the maximal diastolic potential at around -60 mV is primarily produced by I_<Kr> and that the contribution of I_<Kr> to the late repolarization is either absent or, if any, very small in spontaneous action potentials in guinea-pig SA node cells. While the present study did not fully elucidate the role of I_<Ks> in the spontaneous action potentials, it is reasonable to speculate that I_<Ks> is, at least in part, responsible for the early phase of repolarization in guinea-pig SA node cells. Less

Report

(3 results)
  • 2000 Annual Research Report   Final Research Report Summary
  • 1999 Annual Research Report
  • Research Products

    (9 results)

All Other

All Publications (9 results)

  • [Publications] Omatsu-Kanbe,M.: "Inhibition of store-operated Ca^<2+> entry by extracellular ATP in rat brown adipocytes."J Physiol. 521. 601-615 (1999)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] 松浦博: "心筋活動電位再分極と遅延整流性カリウムチャネルの調節機構."臨牀と研究. 77(4). 134-137 (2000)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] 松浦博: "情報伝達物質としてのATP 自律神経系:心筋イオンチャネル制御."生体の科学. (in press). (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Omatsu-Kanbe, M.: "Inhibition of store-operated Ca^<2+> entry by extracellular ATP in rat brown adipocytes."J Physiol. 521. 601-615 (1999)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] 松浦博: "心筋活動電位再分極と遅延整流性カリウムチャネルの調節機構"臨牀と研究. 77(4). 134-137 (2000)

    • Related Report
      2000 Annual Research Report
  • [Publications] 松浦博: "情報伝達物質としてのATP 自律神経系:心筋イオンチャネル制御"生体の科学. (in press). (2001)

    • Related Report
      2000 Annual Research Report
  • [Publications] Matsubayashi, T.: "On the mechanism of the enhancement of delayed rectifier K^+ current by extracellular ATP in guinea-pig ventricular myocyte"Pflugers Arch. 437. 635-642 (1999)

    • Related Report
      1999 Annual Research Report
  • [Publications] Omatsu-Kanbe, M.: "Inhibition of store-operated Ca^<2+> entry by extracellular ATP in rat brown adipocytes"J Physiol. 521. 601-615 (1999)

    • Related Report
      1999 Annual Research Report
  • [Publications] 松浦 博: "心筋活動電位再分極と遅延整流性カリウムチャネルの調節機構"臨牀と研究. (in press). (2000)

    • Related Report
      1999 Annual Research Report

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Published: 1999-04-01   Modified: 2016-04-21  

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