Depression of ATP-induced Ca2+ signalling by high K+ and low Cl- media in human aortic endothelial cells.
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.
Yumoto
K
K
Cardiovascular Division of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan.
Yamaguchi
H
H
Ochi
R
R
D000255:Adenosine Triphosphate / Q000494:pharmacology*; D001011:Aorta / Q000166:cytology / Q000378:metabolism*; D002118:Calcium / Q000502:physiology*; D002478:Cells, Cultured; D018118:Chloride Channels / Q000502:physiology; D002712:Chlorides / Q000494:pharmacology*; D003470:Culture Media; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism*; D006801:Humans; D009544:Niflumic Acid / Q000494:pharmacology; D009994:Osmolar Concentration; D011188:Potassium / Q000494:pharmacology*; D015221:Potassium Channels / Q000502:physiology; D015398:Signal Transduction / Q000187:drug effects*
D018118:Chloride Channels; D002712:Chlorides; D003470:Culture Media; D015221:Potassium Channels; D009544:Niflumic Acid; D000255:Adenosine Triphosphate; D011188:Potassium; D002118:Calcium