Chloride secretion by canine tracheal epithelium: II. The cellular electrical potential profile

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Abstract
We used intracellular microelectrode techniques to study the mechanisms responsible for Cl secretion by canine tracheal epithelium. Tissues were treated with indomethacin (10−6 m, added to the mucosal solution) to reduce the baseline rate of Cl secretion and then stimulated by addition of epinephrine (10−6 m) or prostaglandin E1 (10−6 m) to the submucosal solution. Three conclusions emerged from our findings: First, secretagogues enhance the rate of transepithelial Cl transport primarily by increasing apical membrane Cl permeability, since: (i) stimulation of secretion produced parallel decreases in transepithelial resistance (R t) and the membrane resistance ratioR a/Rb, whereR a andR b refer to the resistances of the apical and basolateral membranes; (ii) there was an inverse relation between the short-circuit current andR a/Rb; (iii) secretagogues depolarized the electrical potential difference across the apical membrane (ψa) and produced an equivalent hyperpolarization of the transepithelial electrical potential difference (ψ1) so that, in the steady-state, the basolateral membrane potential (ψb) was unchanged; and (iv) substitution of sulfate or gluconate for Cl in the bathing solutions prevented secretagogue-induced changes inR t, Ra/Rb, (ψa) and (ψ1). Second, Cl entry into the cell across the basolateral membrane appears to be electrically-neutral since omission of Cl from the submucosal solution had no effect on (ψb) and did not decreaseR a/Rb as would be expected if Cl entered the cell by a conductive process. Third, secretagogues decreaseR b. Approximately 20 sec after the onset of the secretory responseR a/Rb underwent a secondary increase whileR t continued to fall. The decrease inR b may reflect an increase in basolateral membrane K permeability.