We have experimented with isolated cardiomyocytes of mollusks Helix. During the whole-cell patch-clamp recordings of K⁺ currents a considerable decrease in amplitude was observed upon repeated voltage steps at 0.96 Hz. For these experiments, ventricular cells were depolarized to identical + 20 mV from a holding potential of − 50 mV. The observed spontaneous inhibition of outward currents persisted in the presence of 4-aminopyridine, tetraethylammonium chloride or E-4031, the selective class III antiarrhythmic agent that blocks HERG channels. Similar tendency was retained when components of currents sensitive to either 4-AP or TEA were mathematically subtracted. Waveforms of currents sensitive to 1 and 10 micromolar concentration of E-4031 were distinct comprising prevailingly those activated during up to 200 ms pulses. The outward current activated by a voltage ramp at 60 mV x s⁻¹ rate revealed an inward rectification around + 20 mV. This feature closely resembles those of the mammalian cardiac delayed rectifier I_Kr.

Graphic Abstract

中文翻译：

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原生 K 通道的失活

我们已经对软体动物Helix 的分离心肌细胞进行了实验。在 K ⁺的全细胞膜片钳记录期间在 0.96 Hz 的重复电压阶跃下观察到电流幅度显着降低。对于这些实验，心室细胞从 - 50 mV 的保持电位去极化至相同的 + 20 mV。在 4-氨基吡啶、四乙基氯化铵或 E-4031（阻断 HERG 通道的选择性 III 类抗心律失常剂）存在下，观察到的外向电流自发抑制持续存在。当以数学方式减去对 4-AP 或 TEA 敏感的电流分量时，保留了类似的趋势。对 1 和 10 微摩尔浓度的 E-4031 敏感的电流波形是不同的，主要包括在高达 200 ms 脉冲期间激活的波形。由 60 mV xs ^-1的电压斜坡激活的外向电流率显示约 + 20 mV 的内向整流。该特征与哺乳动物心脏延迟整流器I _{Kr 的}特征非常相似。

图形摘要