Depression of ATP-Induced Ca2+ Signalling by High K+ and Low Cl- Media in Human Aortic Endothelial Cells.

1 January 1995

journal article
Published by Physiological Society of Japan in The Japanese Journal of Physiology

Vol. 45 (1) , 111-122
https://doi.org/10.2170/jjphysiol.45.111

Abstract

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.

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