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Updated: Jun 3, 2026

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
Published on: July 3, 2013
Allitridi inhibits transient outward potassium currents in human atrial myocytes
Chun-Yu Deng1, Fang Rao, Su-Juan Kuang
1Department of Cardiology, Guangdong Cardiovascular Institute and Guangdong Academy of Medical Sciences, Research Centre of Guangdong General Hospital, Guangzhou, China.
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.
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.
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