Chloride secretion by canine tracheal epithelium: III. Membrane resistances and electromotive forces.

Abstract

We used intracellular microelectrode techniques and equivalent electrical circuit analysis to examine the changes in individual membrane resistances and electromotive forces that accompany stimulation of Cl secretion across canine tracheal epithelium. Tissues were pretreated with indomethacin (10−6 m, mucosal solution) to reduce basel Cl secretion rate. Subsequent addition of epinephrine (10−6 m, submucosal solution) increased the rate of electrogenic Cl secretion as indicated by an increase in the short-circuit current (I sc) and decrease in the transepithelial resistance (R t ). The reduction inR t was due to decreases in bothR a andR b (the resistances of the apical and basolateral cell membranes, respectively). At the apical membrane, a nearly 10-fold decrease inR a was accompanied by reversal of the electromotive force (E a ) from +11±9 mV to −31±3 mV. Variations in Cl secretion rate induced by indomethacin and epinephrine disclosed a direct relation betweenR a andE a . In the presence of indomethacinR a was high andE a was consistent with the chemical potential difference for Na across the apical membrane (ca. +60 mV), reflecting the predominance of Na absorption across indomethacin-treated tissues. In the presence of epinephrine,R a was low andE a was consistent with the chemical potential difference for Cl across this barrier (−31 mV), reflecting the dominance of Cl secretion across epinephrine-treated tissues. These findings suggest that the conversion from absorption to secretion primarily involves a secretogogue-induced decrease in apical membrane resistance to Cl. At the basolateral membrane, epinephrine decreasedR b threefold without markedly altering the electromotive force across this barrier (E b ). To the extent thatR b andE b represent the resistance and chemical potential difference for K diffusion across the basolateral membrane, the inverse relation betweenR b andI sc suggests that stimulation is associated with increased basolateral membrane K permeability without marked changes in intracellular K activity.