Homocysteine inhibits potassium channels in human atrial myocytes
Homocysteine inhibits potassium channels in human atrial myocytes
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DOI：
10.1111/j.1440-1681.2007.04671.x
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发表时间：
2007-09-01
影响因子：
2.9
通讯作者：
Yang, Bao-Feng
中科院分区：
文献类型：
--
作者：
Cai, Ben-Zhi;Gong, Dong-Mei;Yang, Bao-Feng
大量证据表明，同型半胱氨酸（Hcy）水平升高预示着房颤风险增加。然而，关于同型半胱氨酸对心房肌细胞的电生理效应知之甚少。用全细胞膜片钳技术记录人心房肌细胞钾电流，发现50 μ mol/L和500 μ mol/L的同型半胱氨酸（Hcy）使人心房肌细胞瞬间外向钾电流分别降低24.8 ± 5.9和38.4 ± 10.4%。500 μ mol/L Hcy使超快速延迟整流钾电流降低约30%。500 μ mol/L Hcy可使心房肌细胞内向整流钾电流增加约40%，提示Hcy是心房颤动的重要危险因素，可引起心房肌细胞钾电流的电生理紊乱。
A large body of evidence indicates that elevated homocysteine (Hcy) levels portend an increased risk for atrial fibrillation. However, little is known about the electrophysiological effects of Hcy on atrial myocytes. The present study was conducted to investigate the direct effects of Hcy on ion channels in human atria.Whole-cell patch-clamp techniques were used to record potassium currents in human atrial cells.In human atrial myocytes, transient outward potassium currents were significantly decreased by 24.8 +/- 5.9 and 38.4 +/- 10.4% in the presence of 50 and 500 mu mol/L Hcy, respectively. The ultrarapid delayed rectifier potassium currents were decreased by approximately 30% when exposed to 500 mu mol/L Hcy. The inward rectifier potassium currents were increased by approximately 40% in the presence of 500 mu mol/L Hcy.The results of the present study indicate that Hcy, an important risk factor for atrial fibrillation, could cause electrophysiological disturbances of potassium currents in human atrial myocytes.