Yumoto K, Yamaguchi H, Ochi R
Cardiovascular Division of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan.
Jpn J Physiol. 1995;45(1):111-22. doi: 10.2170/jjphysiol.45.111.
We studied the contribution of the Cl- channel as well as K+ channel in the regulation of Ca2+ signalling in fura-2-loaded cultured human aortic endothelial cells. Low Cl- (20 mM) superfusion did not affect the ATP (10 microM)-induced [Ca2+]i increase at the initial peak (control 309 +/- 30 nM (mean +/- SD, n = 17) versus 20 mM [Cl-]o 308 +/- 40 nM (n = 8)) but depressed it at the sustained phase (at 5 min, 170 +/- 29 nM versus 85 +/- 10 nM). Similar selective depression of the sustained phase occurred also in Ca(2+)-free and 140 mM K+ solutions and in the presence of niflumic acid (300 microM), a blocker of the Cl- channel and Ca2+ permeable cation channel. After application of ATP, the increase of [Cl-]o from 20 to 146 mM resulted in a Ca2+ overshoot. Both Cl- and K+ channels play an important role in the regulation of Ca2+ influx presumably by controlling the membrane potential in vascular endothelial cells.
我们研究了氯离子通道以及钾离子通道在调节用fura - 2负载的培养人主动脉内皮细胞中钙离子信号传导方面的作用。低氯（20 mM）灌流在初始峰值时不影响ATP（10 microM）诱导的细胞内钙离子浓度（[Ca2+]i）升高（对照组309±30 nM（平均值±标准差，n = 17），而细胞外氯离子浓度（[Cl-]o）为20 mM时为308±40 nM（n = 8）），但在持续阶段会使其降低（5分钟时，170±29 nM对85±10 nM）。在无钙和140 mM钾离子溶液中以及存在尼氟灭酸（300 microM，一种氯离子通道和钙离子可渗透阳离子通道的阻滞剂）时，也会出现持续阶段的类似选择性降低。施加ATP后，细胞外氯离子浓度从20 mM增加到146 mM会导致钙离子超调。氯离子通道和钾离子通道可能通过控制血管内皮细胞的膜电位在调节钙离子内流中起重要作用。
