Rasmussen H H, TenEick R E, McCullough J R, Singer D H
J Mol Cell Cardiol. 1984 Aug;16(8):771-3. doi: 10.1016/s0022-2828(84)80660-4.
The resting potential of "sodium-loaded' cardiac cells can transiently hyperpolarize to levels negative to the steady state resting potential [3,5,6]. Hyperpolarization is associated with the coupled efflux of Na+ and influx of K+ driven by an active transport process and may result from an increased K+ equilibrium potential (EK), an outward pump current or both. Using conventional microelectrode techniques, we found that Na+-loaded human atrial myocardium can also transiently hyperpolarize. Na+ loading was induced by cooling to 2 degrees to 3 degrees C. Upon rewarming to 37 degrees C in a 20 mM K+ solution, the resting potential transiently hyperpolarized to levels at least 11 mV negative to the calculated EK and 29 +/- 2 mV (mean +/- S.E.) negative to the steady state level (- 33 +/- 2 mV) recorded some 15-20 minutes later. An increase in K+ conductance induced by acetylcholine exposure [2,7,10] during the transient hyperpolarization caused a depolarization, indicating that the resting potential was indeed negative to EK. These findings cannot be explained by either conductance changes or electroneutral Na+ pumping and concomitant extracellular K+ depletion. We conclude that the Na+-loaded human atrium can generate net pump current.
“钠负荷”心肌细胞的静息电位可短暂超极化至比稳态静息电位更负的水平[3,5,6]。超极化与由主动转运过程驱动的Na⁺外流和K⁺内流偶联相关，可能是由于K⁺平衡电位（EK）增加、外向泵电流或两者共同作用所致。使用传统微电极技术，我们发现钠负荷的人心房肌也可短暂超极化。通过冷却至2至3摄氏度诱导钠负荷。在20 mM K⁺溶液中复温至37摄氏度时，静息电位短暂超极化至比计算出的EK至少负11 mV的水平，比约15 - 20分钟后记录的稳态水平（-33±2 mV）负29±2 mV（平均值±标准误）。在短暂超极化期间，乙酰胆碱暴露[2,7,10]诱导的K⁺电导增加导致去极化，表明静息电位确实比EK更负。这些发现无法用电导变化或电中性Na⁺泵浦以及伴随的细胞外K⁺耗竭来解释。我们得出结论，钠负荷的人心脏心房可产生净泵电流。
