Allitridi inhibits transient outward potassium currents in human atrial myocytes

作者：Deng, Chun-Yu; Rao, Fang; Kuang, Su-Juan; Wu, Shu-Lin; Shan, Zhi-Xin; Li, Xiao-Hong; Zhou, Zhi-Ling; Lin, Qiu-Xiong; Liu, Xiao-Ying; Yang, Min; Lin, Shu-Guang; Yu, Xi-Yong^*

来源：CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, 2011, 38(5): 323-327.

DOI：10.1111/j.1440-1681.2011.05511.x

• allitridi
• atrial fibrillation
• human atrium
• ion channels
• transient outward K plus current
• ultrarapid delayed rectifier K plus current

P>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 Ca2+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 mu mol/L). Inactivation of I(to) was accelerated and the voltage-dependent inactivation potential was shifted towards the negative direction. Allitridi (30 mu mol/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.

• 出版日期2011-5
• 单位广东省心血管病研究所; 广东省人民医院