Guerrero S, Zacharias J
Arch Int Pharmacodyn Ther. 1984 May;269(1):94-110.
The effects of 4-aminoquinoline (4-AQ), a drug structurally related to 4-aminopyridine, were studied on atrial contractile fibres from the amphibian Caudiverbera caudiverbera by means of intracellular electrodes. In concentrations that did not change resting potential, 4-AQ (0.25-1.5 mM) reduced upstroke velocity, action potential amplitude (APA) and overshoot in a dose-dependent manner. 4-AQ also prolonged action potential duration (APD) and the fibre effective refractory period (ERP), making the ratio ERP/APD greater than one. These effects were reversible by washing. The drug-induced reduction of upstroke velocity was frequency-dependent. This effect and increase of APD were more intense at higher values of resting potential. All effects produced by 4-AQ remained constant in either high or low external K+ concentrations. The depressant effects of this compound on upstroke velocity, overshoot, APA as well as increase of APD were antagonized by doubling the extracellular Na+ concentration. Data presented support the view that 4-AQ exerts its effects on the frog heart by blocking both sodium and potassium channels, thus causing quinidine-like actions.
通过细胞内电极研究了与4-氨基吡啶结构相关的药物4-氨基喹啉（4-AQ）对两栖动物尾蟾心房收缩纤维的作用。在不改变静息电位的浓度下，4-AQ（0.25-1.5 mM）以剂量依赖性方式降低了去极化速度、动作电位幅度（APA）和超射。4-AQ还延长了动作电位持续时间（APD）和纤维有效不应期（ERP），使ERP/APD比值大于1。这些作用通过冲洗可逆转。药物引起的去极化速度降低与频率有关。这种作用和APD的增加在较高静息电位值时更为明显。在高或低的细胞外K+浓度下，4-AQ产生的所有作用均保持不变。将细胞外Na+浓度加倍可拮抗该化合物对去极化速度、超射、APA的抑制作用以及APD的增加。所提供的数据支持这样的观点，即4-AQ通过阻断钠通道和钾通道对蛙心发挥作用，从而产生类似奎尼丁的作用。
