Guerrero S
Arch Int Pharmacodyn Ther. 1982 Oct;259(2):271-83.
The electrophysiological effects of 4-aminoquinoline (4-AQ), a drug structurally related to 4-aminopyridine, were studied on the sinus venosus of the frog Caudiverbera caudiverbera with standard microelectrode techniques. 4-AQ in concentrations (0.01-1.5 mM) that did not modify membrane resting potential, reversibly depressed pacemaker activity and the rate of diastolic depolarization. These effects were not prevented by atropine. 4-AQ also reduced maximum diastolic potential, whereas action potential amplitude, overshoot and dV/dtmax remained unaffected. Action potential duration was prolonged by 4-AQ in a concentration-related manner by slowing down the repolarization phase. The effects upon repolarization and on diastolic depolarization were abolished by doubling extracellular calcium concentration. They were not suppressed, however, by electrically pacing sinus preparations at the pre-drug frequency. A plausible interpretation of the data is that 4-AQ effects are the consequence of a direct inhibition of potassium conductance at the cell membrane.
采用标准微电极技术，研究了结构与4-氨基吡啶相关的药物4-氨基喹啉（4-AQ）对蛙尾蟾尾静脉窦的电生理效应。浓度为0.01-1.5 mM的4-AQ不会改变膜静息电位，但能可逆性地抑制起搏活动和舒张期去极化速率。这些效应不受阿托品的影响。4-AQ还降低了最大舒张电位，而动作电位幅度、超射值和最大去极化速率（dV/dtmax）不受影响。4-AQ以浓度相关的方式延长动作电位持续时间，其机制是减慢复极化相。细胞外钙浓度加倍可消除对复极化和舒张期去极化的影响。然而，在给药前的频率下对静脉窦标本进行电起搏并不能抑制这些效应。对这些数据的一个合理的解释是，4-AQ的效应是细胞膜钾电导直接受到抑制的结果。
