AJP - Cell Physiology, Vol 258, Issue 4 C630-C638, Copyright © 1990 by American Physiological Society
Potassium conductances in tracheal epithelium activated by secretion and cell swelling
A. G. Butt, W. L. Clapp and R. A. Frizzell
Department of Physiology, University of Alabama, Birmingham 35294.
Increased basolateral membrane K conductance accompanies stimulation of Cl
secretion across canine trachea. To assess the K conductance properties, we
permeabilized the apical membranes with amphotericin B and monitored the
current and conductance caused by K flow across the basolateral membranes.
Under basal unstimulated conditions, two K conductances could be
distinguished by blockers. One was inhibited only by barium; the other was
sensitive also to quinidine and lidocaine. The permeabilities of the basal
conductance pathways to K and Rb were similar (PK/PRb approximately equal
to 1.5). The secretory agonist, epinephrine, selectively increased the
quinidine-insensitive conductance, implicating it in the Cl secretory
response. Cell swelling induced a third conductance with a low permeability
to Rb (PK/PRb approximately equal to 10) that was quinidine sensitive. In
tissues not treated with amphotericin, neither quinidine nor Rb-for-K
replacement inhibited transepithelial Cl secretion. Thus neither of the
quinidine-sensitive K conductances (basal or swelling induced) contribute
to the increase in basolateral K conductance during Cl secretion. Cell
shrinkage inhibited all three conductances and secretion, suggesting that
the initial priority of the cell is volume regulation.
