Electric field-induced functional reductions in the K+ channels mainly resulted from supramembrane potential-mediated electroconformational changes.

The goal of this study is to distinguish the supramembrane potential difference-induced electroconformational changes from the huge transmembrane current-induced thermal damages in the delayed rectifier K+ channels. A double Vaseline-gap voltage clamp was used to deliver shock pulses and to monitor the channel currents. Three pairs of 4-ms shock pulses were used to mimic the electric shock by a power-line frequency electric field. Each pair consists of two pulses with the same magnitude, starting from 350 to 500 mV, but with opposite polarities. The shock pulse-generated transmembrane ion flux and the responding electric energy, the Joule heating, consumed in the cell membrane, as well as the effects on the K+ channel currents, were obtained. Results showed that huge transmembrane currents are not necessary to cause damages in the K+ channel proteins. In contrast, reductions in the K+ channel currents are directly related to the field-induced supramembrane potential differences. By a comparison with the shock field-induced Joule heating effects on cell membranes, the field-induced supramembrane potential difference plays a dominant role in damaging the K+ channels, resulting in electroconformational changes in the membrane proteins. In contrast, the shock field-induced huge transmembrane currents, therefore the thermal effects, play a secondary, trivial role.