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

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 psi a and decreased the fractional resistance of the apical membrane fR. These changes are consistent with an initial increase in apical Cl conductance. In contrast, epinephrine acutely hyperpolarized psi a and increased fR, changes consistent with an initial increase in basolateral K conductance. Following the acute effect of epinephrine, psi a depolarized and fR 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 alpha adrenergic receptors because it was reproduced by addition of the alpha agonist phenylephrine, and blocked by the alpha antagonist phentolamine. The ability of prazosin but not yohimbine to block the acute epinephrine-induced increase in K permeability indicates the presence of alpha 1 adrenergic receptors. The acute alpha 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 beta and alpha adrenergic agents mediate the ion transport processes in canine tracheal epithelium.(ABSTRACT TRUNCATED AT 250 WORDS)