DEPRESSION OF ATP-INDUCED CA2- MEDIA IN HUMAN AORTIC ENDOTHELIAL-CELLS( SIGNALING BY HIGH K+ AND LOW CL)

We studied the contribution of the Cl- channel as well as K+ channel i n the regulation of Ca2+ signalling in fura-2-loaded cultured human ao rtic endothelial cells. Low Cl- (20 mM) superfusion did not affect the ATP (10 mu M)-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 v ersus 85+/-10 nM). Similar selective depression of the sustained phase occurred also in Ca2+-free and 140 mM K+ solutions and in the presenc e of niflumic acid (300 mu M), a blocker of the Cl- channel and Ca2+ p ermeable cation channel. After application of ATP, the increase of [Cl -](o) from 20 to 146 mM resulted in a Ca2+ overshoot. Both Cl- and Kchannels play an important role in the regulation of Ca2+ influx presu mably by controlling the membrane potential in vascular endothelial ce lls.