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MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS

Activation of chloride currents in murine portal vein smooth muscle cells by membrane depolarization involves intracellular calcium release

Department of Basic Medical Sciences, Pharmacology and Clinical Pharmacology, St. George's Hospital Medical School, London, United Kingdom

Submitted 9 August 2004 ; accepted in final form 2 September 2004

The present study describes the first characterization of Ca²⁺-activated Cl^– currents (I_ClCa) in single smooth muscle cells from a murine vascular preparation (portal veins). I_ClCa was recorded using the perforated patch version of the whole cell voltage-clamp technique and was evoked using membrane depolarization. Generation of I_ClCa relied on Ca²⁺ entry through dihydropyridine-sensitive Ca²⁺ channels because I_ClCa was abolished by 1 µM nicardipine and enhanced by raising external Ca²⁺ concentration or by application of BAY K 8644. I_ClCa was characterized by the sensitivity to Cl^– channel blockers and the effect of altering the external anion on reversal potential. Activation of I_ClCa after membrane depolarization was dependent on Ca²⁺ release from intracellular stores. Thus the amplitude of I_ClCa was diminished by the SR-ATPase inhibitor cyclopiazonic acid, the inositol 1,4,5-trisphosphate receptor antagonist 2-aminoethoxydiphenyl borate (2-APB), and the ryanodine receptor blocker tetracaine. The degree of inhibition produced by the application of 2-APB and tetracaine together was significantly greater than the effect of each agent applied alone. In current-clamp mode, injection of depolarizing current elicited a biphasic action potential, with the later depolarization being sensitive to niflumic acid (NFA; 10 µM). In isometric tension recordings, NFA inhibited spontaneous contractions. These data support a role for this conductance in portal vein excitability.

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