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

• Published in: The Journal of physiology Vol. 516; no. 2; p. 365
• Main Authors: I A Greenwood, W A Large
• Format: Journal Article
• Language: English
• Published: The Physiological Society 15.04.1999
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1111/j.1469-7793.1999.0365v.x

The effects of external anions on the decay kinetics of Ca 2+ -activated Cl − currents ( I Cl(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 Ca 2+ -activated Cl − currents (STICs) and Ca 2+ -activated Cl − ‘tail’ currents ( I tail ) 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 I tail . There was a positive correlation between the ability of an external anion to affect the decay τ of I Cl(Ca) and its permeability relative to Cl − . The voltage dependence of STIC and I tail decay was not affected by external or internal anions. External permeating anions were not obligatory for activation of I Cl(Ca) and STIC τ was not altered in Cl − -free external solution. 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. In conclusion, external anions affect the decay of I Cl(Ca) by a mechanism compatible with an interaction with a binding site which modulates Cl − channel kinetics.