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アイテム

  1. Public
  2. 研究紀要
  3. ACTA MEDICA KINDAI UNIVERSITY
  4. 23(1/2)1998

SD-3212 blocks the inward rectifier potassium channel in guinea pig ventricular myocytes

https://kindai.repo.nii.ac.jp/records/2002965
https://kindai.repo.nii.ac.jp/records/2002965
2b8958ac-5ed5-4605-acb9-f825c9759337
名前 / ファイル ライセンス アクション
AA0050842X-19980600-0001.pdf AA0050842X-19980600-0001.pdf (638.4 KB)
アイテムタイプ 紀要論文 / departmental bulletin paper(1)
公開日 2025-06-20
タイトル
タイトル SD-3212 blocks the inward rectifier potassium channel in guinea pig ventricular myocytes
言語 en
作成者 Akamatsu, Kan-Ichiro

× Akamatsu, Kan-Ichiro

en Akamatsu, Kan-Ichiro
Kinki University

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Takai, Hiroyuki

× Takai, Hiroyuki

en Takai, Hiroyuki
Kinki University

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Izawa, Hiroshi

× Izawa, Hiroshi

en Izawa, Hiroshi
Kinki University

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Ishikawa, Kinji

× Ishikawa, Kinji

en Ishikawa, Kinji
Kinki University

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言語
言語 eng
キーワード
主題 inward rectifier potassium channel, SD-3212, ventricular myocytes
内容記述
内容記述タイプ Abstract
内容記述 SD-3212 inhibited the calcium current, the sodium current and the muscarinic acetylcholine-receptor-operated potassium current. Inward rectifier potassium current (IK1)is considered to contribute to both the repolarization phase of the ventricular action potential and the maintenance of the resting potential. However, the kinetics of blocking effects of multiple channel blockers on the IK1 are unclear. In the present study, we investigated the effects of SD-3212 on the IK1 channel in isolated guinea pig ventricular myocytes. Male guinea pig heart was perfused by Langendorff's method to prepare isolated ventricular myocytes using collagenase. Membrane currents of the isolated ventricular myocytes were recorded using the patch clamp technique. The peak and steady-state IK1 were constantly inhibited by 100μM SD-3212 irrespective of the potentials applied (the steady-state current was 36±4% blocked and the peak current was 28±2% blocked) under whole cell clamp conditions. Slope conductance 35±3pS was unchanged. SD-3212 (1mM) decreased the open probability from 92.5±0.8% in the control to 90.2±l.8% after 2 min, 85.5±2.4% after 3 min, 64.7±3.2% after 4 min, and to 22.6±2.4% after 5 min of exposure. Mean open time and mean closed time were unchanged after 5 min of exposure. SD-3212 decreased the open probability from 92.5±0.8% under control conditions to 91.6±1.4% in the presence of 100μM SD-3212, 63.3±2.4% with 500μM SD-3212 and 22.6±3.1% with 1mM SD-3212 after 5 min of exposure under single channel recordings. In conclusions, SD-3212 blocks the IK1 channels in a high dose concentration-dependent manner. SD-3212 blocks IK1 channels via a hydrophobic pathway in accordance with a slow blocking mode.
言語 en
出版者
出版者 The Kinki University Medical Association
言語 en
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ departmental bulletin paper
出版タイプ
出版タイプ AM
出版タイプResource http://purl.org/coar/version/c_ab4af688f83e57aa
収録物識別子
収録物識別子タイプ PISSN
収録物識別子 03866092
開始ページ
開始ページ 1
終了ページ
終了ページ 8
書誌情報 en : ACTA MEDICA KINKI UNIVERSITY

巻 23, 号 1/2, p. 1-8, 発行日 1998-06
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