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

Summary

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/R_b, 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/R_b; (iii) secretagogues depolarized the electrical potential difference across the apical membrane (ψ_a) and produced an equivalent hyperpolarization of the transepithelial electrical potential difference (ψ₁) so that, in the steady-state, the basolateral membrane potential (ψ_b) was unchanged; and (iv) substitution of sulfate or gluconate for Cl in the bathing solutions prevented secretagogue-induced changes inR _t, R_a/R_b, (ψ_a) 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 (ψ_b) and did not decreaseR _a/R_b 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/R_b underwent a secondary increase whileR _t continued to fall. The decrease inR _b may reflect an increase in basolateral membrane K permeability.