Bondarenko O I, Sahach V F
A. A. Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kiev.
Fiziol Zh (1994). 1998;44(5-6):14-20.
The changes in the membrane potential (MP) of in situ endothelial cells from guinea pig aorta was studied using patch-champ technique under ATP stimulation. Extracellular ATP is shown to evoke the complex changes in endothelial MP: initial short-lived depolarization and subsequent maintained hyperpolarization. Extracellular calcium buffering as well as addition of extracellular Ni2+ made the hyperpolarization shorter. After the buffering of intracellular calcium ATP addition evoked only depolarization which was not observed in the absence of extracellular sodium. The hyperpolarization under ATP stimulation was absent after emptying of intracellular calcium stores. It was concluded that hyperpolarization in response to ATP is initiated by calcium release from intracellular stores followed by activation of calcium-dependent potassium channels, the maintained phase of hyperpolarization is provided by extracellular calcium entry and initial depolarization by extracellular sodium entry into EC.
采用膜片钳技术研究了豚鼠主动脉原位内皮细胞膜电位（MP）在ATP刺激下的变化。结果表明，细胞外ATP可引起内皮细胞MP的复杂变化：最初短暂的去极化和随后持续的超极化。细胞外钙缓冲以及添加细胞外Ni2+使超极化时间缩短。细胞内钙缓冲后，添加ATP仅引起去极化，而在无细胞外钠的情况下未观察到这种情况。细胞内钙库排空后，ATP刺激下的超极化消失。得出的结论是，ATP引起的超极化是由细胞内钙库释放钙引发的，随后激活钙依赖性钾通道，超极化的持续阶段由细胞外钙内流提供，而最初的去极化是由细胞外钠进入内皮细胞引起的。
