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The effects of external anions on the decay kinetics of Ca2+-activated Cl- currents (ICl(Ca)) were studied in smooth muscle cells isolated from rabbit portal vein using the perforated patch whole-cell voltage clamp technique.
In normal NaCl-containing external solution the decay of spontaneous Ca2+-activated Cl- currents (STICs) and Ca2+-activated Cl- 'tail' currents (Itail) was described by a single exponential with a time constant (
) that was prolonged by external anions which are more permeable than Cl- (Br-, I- and SCN-) and accelerated by less permeant anions. However, intracellular I- did not affect the of STICs and Itail.
There was a positive correlation between the ability of an external anion to affect the decay of ICl(Ca) and its permeability relative to Cl-.
The voltage dependence of STIC and Itail decay was not affected by external or internal anions.
External permeating anions were not obligatory for activation of ICl(Ca) and STIC was not altered in Cl--free external solution.
Modulation of by mole fractions of SCN- and Cl- ions was fitted by a logistic curve, suggesting competition between SCN- and Cl- ions for a binding site.
In conclusion, external anions affect the decay of ICl(Ca) by a mechanism compatible with an interaction with a binding site which modulates Cl- channel kinetics.
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