Chen Hui, Zhang Dong, Hua Ren Jiang, Ping Chao Sheng
Department of Cardiology, Pu Ai Hospital of Wuhan City, Wuhan 430034, China. ; Department of Cardiology, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Department of Cardiology, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Iran J Pharm Res. 2013 Fall;12(4):855-66.
The goal of this study was to determine the effects of the L-type calcium channel blockers verapamil and diltiazem on the currents of voltage-gated potassium channel (fKv1.4ΔN), an N-terminal-deleted mutant of the ferret Kv1.4 potassium channel. Measurements were made using a two electrode voltage clamp technique with channels expressed stably in Xenopus oocytes. The fKv1.4ΔN currents displayed slow inactivation, with a half-inactivation potential of -38.38 mV and slow recovery from inactivation (τ = 1.90 seconds at -90 mV). The fKv1.4ΔN currents exhibited state-dependent blockade by both drugs, and the inhibition was frequency-, voltage-, and concentration-dependent, consistent with open channel block. Verapamil and diltiazem blocked fKv1.4ΔN currents with 50% inhibitory concentration (IC50) values of 260.71 ± 18.50 μmol/L and 241.04 ± 23.06 μmol/L, respectively. Verapamil accelerated the C-type inactivation rate and slowed recovery of the fKv1.4Δ N channel, while shifting the steady activation curve to the right. Blockade of fKv1.4ΔN currents by diltiazem was similar to that of verapamil, but diltiazem accelerated the decay rate of inactivation of fKv1.4ΔN currents without modifying the kinetics of current activation. The present results suggest that verapamil and diltiazem accelerate the C-type inactivation and slow the recovery of the fKv1.4ΔN channel in the open state.
本研究的目的是确定L型钙通道阻滞剂维拉帕米和地尔硫䓬对电压门控钾通道(fKv1.4ΔN)电流的影响,fKv1.4ΔN是雪貂Kv1.4钾通道的N端缺失突变体。使用双电极电压钳技术进行测量,通道在非洲爪蟾卵母细胞中稳定表达。fKv1.4ΔN电流表现出缓慢失活,半失活电位为-38.38 mV,失活后恢复缓慢(在-90 mV时τ = 1.90秒)。两种药物对fKv1.4ΔN电流均表现出状态依赖性阻断,且抑制作用具有频率、电压和浓度依赖性,符合开放通道阻断。维拉帕米和地尔硫䓬阻断fKv1.4ΔN电流的50%抑制浓度(IC50)值分别为260.71±18.50 μmol/L和241.04±23.06 μmol/L。维拉帕米加快了fKv1.4ΔN通道的C型失活速率并减慢了其恢复,同时将稳态激活曲线向右移动。地尔硫䓬对fKv1.4ΔN电流的阻断作用与维拉帕米相似,但地尔硫䓬加快了fKv1.4ΔN电流失活的衰减速率,而未改变电流激活的动力学。目前的结果表明,维拉帕米和地尔硫䓬可加快fKv1.4ΔN通道在开放状态下的C型失活并减慢其恢复。