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Vancouver Vascular Biology Research Center and Department of Pharmacology and Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3
The effect of extracellular
Cl
in regulating
ACh-induced Ca2+ entry into
freshly isolated rabbit aortic endothelial cells was studied using
Ca2+-sensitive fluorescence
microscopy and patch-clamp electrophysiology. After ACh caused
transient Ca2+ release in
Ca2+-free medium, readdition of 3 mM Ca2+ to the bath maintained
Ca2+ entry. Removal of
extracellular Cl abolished
the plateau phase in Ca2+ signal
and inhibited divalent cation entry. However, in the presence of the
K+ ionophore valinomycin, removal
of Cl had no effect on the
Ca2+ plateau. Under current-clamp
conditions, substitution of gluconate for
Cl induced membrane
depolarization. Under voltage clamp, with CsCl in the pipette, ACh
activated a slowly developing
Cl current, which was
blocked by SITS and 5-nitro-2-(3-phenylpropylamino)benzoic acid.
Varying the membrane potential by utilizing different extracellular K+ concentrations in the presence
of 5 µM valinomycin demonstrated that depolarization blocked
ACh-stimulated Mn2+ entry. These
data suggest that ACh-induced Ca2+
entry in freshly isolated endothelial cells requires the presence of
extracellular Cl to
maintain a polarized membrane potential.
chloride; receptor-operated channel; calcium influx; endothelium
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