Electrophysiology of Cl secretion in canine trachea

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Abstract
Conventional microelectrode techniques were employed to determine the mechanism of Cl secretion by canine tracheal epithelium. Epinephrine, a potent stimulator of Cl secretion in these cells, hyperpolarized both the transepithelial potential (20 to 38.9 mV) and the potential across the basolateral membrane (−63.9 to −68.2 mV) and depolarized the potential across the apical membrane (−43.9 to −29.3 mV). Epinephrine also caused a decrease in the transepithelial resistance and ratio of apical to apical+basolateral membrane resistances (777 to 379 Ωcm2 and 0.71 to 0.35, respectively) though the change in the latter was biphasic, first decreasing then slightly increasing. Ionic substitutions, either Na, K or Cl, in the mucosal bathing solutions were found to cause changes in the resistances and potentials measured. In the presence of epinephrine, the changes produced by the Na and K substitutions decreased, while those produced by altering the mucosal Cl concentration increased. A model was designed to analyze the results from these experiments. When used in conjunction with the Goldman-Hodgkin-Katz equation, the results from this model indicate that epinephrine caused a large increase in the Cl permeability of the apical membrane of the cell. From these results we conclude that the increase in Cl secretion caused by epinephrine is accompanied by at least two cellular events: the primary event is an increase in the Cl conductance of the apical membrane; the second event is either an increase in the conductance of the basolateral membrane (probably due to an increase in K permeability) or an increase in shunt conductance or a combination of both.