Zünkler B J, Henning B, Gräfe M, Bass R, Hildebrandt A G, Fleck E
Federal Institute for Drugs and Medical Devices, Berlin, FRG.
Basic Res Cardiol. 1995 Nov-Dec;90(6):435-42. doi: 10.1007/BF00788535.
The electrophysiological properties of human coronary endothelial cells (HCEC) of macro- and microvascular origin were studied using the whole-cell configuration of the patch-clamp technique. The membrane potential of confluent HCEC (-41.9 +/- 3.9 mV (mean +/- SEM, n = 32) for macro- and -33.6 +/- 2.6 mV (n = 64) for microvascular cells, respectively) was less negative than the K+ equilibrium potential. Inward currents of isolated cells at potentials below the K+ equilibrium potential were blocked by external Ba2+ (1 mM), inactivated due to time- and voltage-dependent block caused by external Na+, and their amplitudes were enhanced by increasing extracellular [K+]; these currents were identified as inwardly rectifying K+ currents. Some isolated cells displayed outwardly directed K+ currents which were abolished after replacement of Cs+ for K+ on both sides of the membrane. Voltage-dependent Ca2+ currents could not be observed in isolated HCEC. Hyperpolarizations induced by vasoactive agonists have been observed in some endothelial cells from different species. In contrast, extracellularly applied ATP (adenosine-5'-triphosphate) and ADP (adenosine-5'-diphosphate) at micromolar concentrations depolarized confluent HCEC, whereas adenosine had no effect on resting potentials (RP), indicating that the nucleotide-induced depolarizations were mediated via P2- purinoceptors. These depolarizations occurred even after replacement of N-methyl-D-glucamine for extracellular Na+, indicating that Ca(2+)-influx was involved. There were no marked differences in the electrophysiological properties between cells of macro and microvascular origin.
采用膜片钳技术的全细胞模式，研究了源自大、微血管的人冠状动脉内皮细胞（HCEC）的电生理特性。汇合的HCEC的膜电位（大血管来源的细胞为-41.9±3.9 mV（平均值±标准误，n = 32），微血管来源的细胞为-33.6±2.6 mV（n = 64））比K⁺平衡电位的负值小。在低于K⁺平衡电位的电位下，分离细胞的内向电流被外部Ba²⁺（1 mM）阻断，因外部Na⁺引起的时间和电压依赖性阻断而失活，并且其幅度因细胞外[K⁺]增加而增强；这些电流被鉴定为内向整流K⁺电流。一些分离的细胞表现出外向的K⁺电流，在膜两侧用Cs⁺替代K⁺后该电流消失。在分离的HCEC中未观察到电压依赖性Ca²⁺电流。在不同物种的一些内皮细胞中观察到血管活性激动剂诱导的超极化。相反，微摩尔浓度的细胞外应用ATP（腺苷-5'-三磷酸）和ADP（腺苷-5'-二磷酸）使汇合的HCEC去极化，而腺苷对静息电位（RP）无影响，表明核苷酸诱导的去极化是通过P2嘌呤受体介导的。即使在用N-甲基-D-葡糖胺替代细胞外Na⁺后这些去极化仍会发生，表明涉及Ca²⁺内流。源自大、微血管的细胞在电生理特性上没有明显差异。
