Evidence for voltage-sensitive, calcium-conducting channels in
airway epithelial cells.
Boitano, Scott, Michael L. Woodruff, Ellen R. Dirksen.
Department of Neurobiology, 73-235CHS, UCLA School of Medicine, Box
951763, Los Angeles, California 90095-1763
APStracts 2:0271C, 1995.
In airway epithelial cultures, mechanical stimulation induces [Ca2-]i
changes by causing Ca2- entry and intracellular Ca2- release.
Mechanically-induced Ca2- fluxes across the plasma membrane are
blocked by Ni2- (Boitano et al., 1994). In this report we use
fluorescence imaging microscopy with fura-2 and intracellular
recording of the transmembrane potential to further characterize Ca2-
flux in the plasma membrane of these cells. Mechanically-induced Ca2-
influx is blocked by nifedipine. Addition of the dihydropyridine
agonist Bay-K8644 (2 [mu]M) leads to a delayed increase of
intracellular Ca2- concentration ([Ca2-]i) that is dependent on
extracellular Ca2-. Switching to high extracellular K- concentration
([K-]o) causes depolarization of the plasma membrane and a transient
increase in [Ca2- ]i. The number of cells that respond to high [K-]o
is significantly decreased by Ni2- (1 mM) or nifedipine (10 [mu]M).
Mechanical stimulation causes a rapid depolarization of the
stimulated cell that can be suppressed by the K--ionophore
valinomycin. Valinomycin treatment also blocks mechanically-induced
Ca2- flux. These results suggest that voltage-sensitive Ca2-
-conducting channels exist in airway epithelial cells and these
channels contribute to the [Ca2-]i changes observed following
mechanical stimulation or depolarization of the plasma membrane.
Received 21 November 1994; accepted in final form 6 July 1995.
APS Manuscript Number C680-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 July 1995.