Ca2+-dependent cl_ current in canine tracheal smooth muscle cells. Janssen, Luke J., and Stephen M. Sims. Department of Physiology, University of Western Ontario, London, Ontario, Canada N6A 5C1
APStracts 2:0079C, 1995.
Our goal was to investigate the role of Ca2+ entry in regulating chloride current in smooth muscle cells from canine trachealis. When studied using the perforated patch configuration, depolarization elicited a dihydropyridine-sensitive Ca2+ current (ICa), followed in many cells by a sustained current. This sustained current reversed direction close to the Cl_ equilibrium potential, consistent with it representing Cl_ current. The Cl_ current was also apparent as slowly-deactivating tail currents seen upon repolar ization to negative potentials. The Cl_ channel blocker niflumic acid abolished both the sustained and tail currents, without affecting ICa. Several observations indicated that the Cl_ current was dependent on Ca2+ entry. ICl was increased in magnitude when Ca2+ influx was augmented (by prolonging the depolarization or using Bay K 8644 or acetylcholine) and decreased in magnitude when Ca2+ influx was reduced (using nifedipine). Based on these findings, we conclude that depolarization causes Ca2+ entry, with resultant elevation of cytosolic free [Ca2+] leading to activation of Cl_ current (ICl(Ca)). We investigated whether Ca2+-induced Ca2+ release from the sarcoplasmic reticulum was involved in activation of ICl(Ca), by depleting intracellular stores of Ca2+ using cyclopiazonic acid to block the sarcoplasmic Ca2+-ATPase and repeated stimulation with acetylcholine (ACh). In such Ca2+-depleted cells, depolarization -mediated Ca2+ entry continued to activate ICl(Ca), suggesting that Ca2+-induced Ca2+ release was not required for its activation. We conclude that Ca2+ entry can activate Cl_ channels in tracheal smooth muscle. This represents a positive feedback system, which would promote excitation and contraction of airway muscle. 

Received 30 June 1994; accepted in final form 18 January 1995
APS Manuscript Number C374-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 28 February 1995.