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Allitridi inhibits transient outward potassium currents in human atrial myocytes
Author(s) -
Deng ChunYu,
Rao Fang,
Kuang SuJuan,
Wu ShuLin,
Shan ZhiXin,
Li XiaoHong,
Zhou ZhiLing,
Lin QiuXiong,
Liu XiaoYing,
Yang Min,
Lin ShuGuang,
Yu XiYong
Publication year - 2011
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2011.05511.x
Subject(s) - atrial myocytes , myocyte , repolarization , medicine , chemistry , cardiac transient outward potassium current , inward rectifier potassium ion channel , atrial action potential , electrophysiology , patch clamp , biophysics , potassium channel , endocrinology , cardiology , ion channel , biology , receptor
Summary 1. It has been reported that allitridi, an active compound extracted from garlic, has many cardiovascular effects. However, it remains unknown whether allitridi affects major repolarization currents, such as the transient outward K + current ( I to ), ultrarapid delayed rectifier K + current ( I Kur ) and the L‐type Ca 2+ current ( I Ca ), in human atrial myocytes. 2. In the present study, we investigated the effects of allitridi on I to , I Kur , I Ca and the action potential in human isolated atrial myocytes using the whole‐cell patch recording technique. 3. Allitridi reversibly inhibited I to , but not I Kur and I Ca , in human atrial myocytes. These effects of allitridi on I to were concentration dependent (IC 50 = 44.9 μmol/L). Inactivation of I to was accelerated and the voltage‐dependent inactivation potential was shifted towards the negative direction. Allitridi (30 μmol/L) significantly prolonged action potential duration in human atrial myocytes. 4. The results of the present study indicate that allitridi inhibits I to , but not I Kur and I Ca , and prolongs the action potential duration in human atrial myocytes.