AJP - Cell Physiology, Vol 254, Issue 4 C519-C525, Copyright © 1988 by American Physiological Society
Effect of a chloride channel blocker on bullfrog corneal epithelium
J. I. Scheide and J. A. Zadunaisky
Department of Physiology, New York University Medical Center, New York 10016.
The effect of the chloride channel blocker, diphenylamine-2-carboxylate
(DPC), was investigated on the bullfrog cornea epithelium using
microelectrodes. Perfusion of 2 X 10(-4) M DPC on the tear side resulted in
a 44% reduction of the corneal transepithelial potential difference (TEP)
and a 9% reduction in corneal conductance. The cornea epithelial cells
hyperpolarized 7.2 +/- 1.5 mV, and the apical fractional resistance
increased 35% (n = 8 tissues). The basolateral potential difference
depolarized 5.5 +/- 1.8 mV. The relative apical conductance decreased 29%,
whereas relative changes of basolateral membranes increased 56% with
prolonged DPC exposure, indicating that the DPC inhibition was acting at
the apical cell membrane. DPC-treated corneas could be stimulated with
isoproterenol (10(-6) M), indicating that the DPC inhibition could be
reversed with the stimulation of chloride conductance. The DPC inhibitory
effect was dependent on basolateral chloride. Intracellular chloride
activity increases with DPC, indicating that the integrity of the
basolateral chloride entry mechanism was not altered. The DPC inhibitory
action was due to a reduction in apical chloride conductance.
