Adrenergic stimulation of Na⁺ transport across alveolar epithelial cells involves activation of apical Cl^- channels

Alveolar epithelial cells were isolated from adult Sprague-Dawley rats and grown to confluence on membrane filters. Most of the basal short-circuit current (I(sc); 60%) was inhibited by amiloride (IC₅₀ 0.96 μM) or benzamil (IC₅₀ 0.5 μM). Basolateral addition of terbutaline (2 μM) produced a rapid decrease in I(sc), followed by a slow recovery back to its initial amplitude. When Cl^- was replaced with methanesulfonic acid, the basal I(sc) was reduced and the response to terbutaline was inhibited. In permeabilized monolayer experiments, both terbutaline and amiloride produced sustained decreases in current. The current-voltage relationship of the terbutaline- sensitive current had a reversal potential of -28 mV. Increasing Cl^- concentration in the basolateral solution shifted the reversal potential to more depolarized voltages. These results were consistent with the existence of a terbutaline-activated Cl^- conductance in the apical membrane. Terbutaline did not increase the amiloride-sensitive Na⁺ conductance. We conclude that β-adrenergic stimulation of adult alveolar epithelial cells results in an increase in apical Cl^- permeability and that amiloride- sensitive Na⁺ channels are not directly affected by this stimulation.