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The action of adrenergic agonists on ion fluxes across the epithelium of the canine trachea was determined. Isolated sheets of tracheal mucosal membranes were mounted in Ussing-type chambers, bathed with Krebs-Henseleit solution at 37 degrees C, pH 7.4, and gassed with 5% CO2 Iin oxygen. Various adrenergic agents, when added to the bathing medium elevated short-circuit current (SCC) (isoproterenol greater than epinephrine greater than norepinephrine greater than phenylephrine). Propranolol (10(-6) M) decreased SCC response to epinephrine. Epinephrine (1mM) increased both unidirectional 36Cl fluxes; net 36Cl secretion toward the lumen increased from 2.01 +/- 0.52 to 3.20 +/- 0.46 mueg/cm2.h (P less than 0.05); 22Na flux did not change. In epinephrine-stimulated tissues, propranolol (1mM) abolished net 36Cl secretion. The SCC response to epinephrine was blunted in the absence of Na from the submucosal reservoir; this blunting suggests that Cl entry across the basal membrane is coupled with Na. Both the relative sensitivities of SCC to various adrenergic agonists and the effect of propranolol suggest that Cl-secretory process is highly sensitive to beta-adrenergic receptor stimulation. Epinephrine increased cell membrane permeability to Cl and probably stimulated a specific Cl pump.
Al-Bazzaz et al. (Wed,) studied this question.