N-n-Butyl haloperidol iodide inhibits the augmented Na⁺/Ca²⁺ exchanger currents and L-type Ca²⁺ current induced by hypoxia/reoxygenation or H₂O₂ in cardiomyocytes

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• 作者：Yongpan Huang^a ; Fenfei Gao^a ; Yanmei Zhang^a ; Yicun Chen^a ; Bin Wang^a ; Yanshan Zheng^a ; Ganggang Shi^a ; ^b ; ^{yongpanhuangxy@yahoo.cn} ; ^{ggshi@stu.edu.cn}
• 关键词：N-n-butyl haloperidol iodide ; Na+/Ca2+ exchanger currents ; L-type Ca2+ current ; Ventricular myocytes ; Patch-clamp techniques
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2012
• 期刊代码：159_0006291x
• 类别：bio
• 出版时间：27 April, 2012
• 卷：421
• 期：1
• 页码：86-90
• 文件大小：568 K

摘要

N-n-butyl haloperidol iodide (F₂), a novel quaternary ammonium salt derivative of haloperidol, was reported to antagonize myocardial ischemia/reperfusion injuries. To investigate its mechanisms, we characterized the effects of F₂ on Na⁺/Ca²⁺ exchanger currents (I_NCX) and the L-type Ca²⁺ channel current (I_Ca,L) of cardiomyocytes during either hypoxia/reoxygenation or exposure to H₂O₂. Using whole-cell patch-clamp techniques, the I_NCX and I_Ca,L were recorded from isolated rat ventricular myocytes. Exposure of cardiomyocytes to hypoxia/reoxygenation or H₂O₂ enhanced the amplitude of the inward and outward of I_NCX and I_Ca,L. F₂ especially inhibited the outward current of Na⁺/Ca²⁺ exchanger, as well as the I_Ca,L, in a concentration-dependent manner. F₂ inhibits cardiomyocyte I_NCX and I_Ca,L after exposure to hypoxia/reoxygenation or H₂O₂ to antagonize myocardial ischemia/reperfusion injury by inhibiting Ca²⁺ overload.