Adrenergic regulation of ion transport by primary cultures of canine tracheal epithelium: Cellular electrophysiology

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Abstract
We examined the effect of adrenergic agents on the cellular electrical properties of primary cultures of canine tracheal epithelium. Both isoproterenol and epinephrine stimulated Cl secretion, as evidenced by an increase in transepithelial voltage and a fall in transepithelial resistance. Moreover, both agents appear to increase the conductance of apical and basolateral membranes. However, the pattern of response was different. Isoproterenol initially depolarized apical voltage Ψ a and decreased the fractional resistance of the apical membranef R. These changes are consistent with an initial increase in apical Cl conductance. In contrast, epinephrine acutely hyperpolarized Ψ a and increasedf R, changes consistent with an initial increase in basolateral K conductance. Following the acute effect of epinephrine, Ψ a depolarized andf R decreased to values not significantly different from those observed with isoproterenol. The acute increase in basolateral K conductance produced by epinephrine appeared to result from stimulation of α adrenergic receptors because it was reproduced by addition of the α agonist phenylephrine, and blocked by the α antagonist phentolamine. The ability of prazosin but not yohimbine to block the acute epinephrine-induced increase in K permeability indicates the presence of α1 adrenergic receptors. The acute α adrenergic-induced increase in basolateral K conductance may be mediated by an increase in cell Ca because the response was mimicked by addition of the Ca ionophore A23187. In contrast, the response to isoproterenol was similar to that observed with addition of 8-bromo-cAMP and theophylline. These results indicate that both β and α adrenergic agents mediate the ion transport processes in canine tracheal epithelium. β adrenergic agents have their primary effect on the apical Cl conductance, probably via an increase in cAMP. α adrenergic agents exert their primary effect on the basolateral K conductance, possibly via an increase in cell Ca.