Modulation of the decay of Ca2+‐activated Cl− currents in rabbit portal vein smooth muscle cells by external anions

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Abstract
1 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. 2 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 (τ) 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 τ of STICs and Itail. 3 There was a positive correlation between the ability of an external anion to affect the decay τ of ICl(Ca) and its permeability relative to Cl−. 4 The voltage dependence of STIC and Itail decay was not affected by external or internal anions. 5 External permeating anions were not obligatory for activation of ICl(Ca) and STIC τ was not altered in Cl−‐free external solution. 6 Modulation of τ 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. 7 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.