The effect of β-adrenergic receptor stimulation on Cl− channel activation was investigated in alveolar epithelial cells grown in monolayer culture and in freshly isolated cells. Monolayers cultured under apical air interface conditions exhibited enhanced amiloride-sensitive Na+ transport compared to apical liquid interface monolayers. Amiloride or benzamil inhibited most (66%) of the basal short circuit current (Isc) with half-maximal inhibitory concentration (IC 50) values of 0.62 μm and 0.09 μm respectively. Basolateral addition of terbutaline (2 μm) produced a rapid decrease in Isc followed by a slow recovery that exceeded the basal Isc. When Cl− was replaced with methanesulfonate in either intact monolayers or basolateral membrane permeabilized monolayers, the response to terbutaline (2 μm) was completely inhibited. No effect of terbutaline on amiloride-sensitive Na+ current was detected. β-Adrenergic agonists and 8-chlorothiophenyl cyclic adenosine monophosphate (8-ctp cAMP) directly stimulated a Cl− channel in freshly isolated alveolar epithelial cells. The current was blocked by glibenclamide (100 μm) and had a reversal potential of −22 mV. No increase in amiloride-sensitve current was detected in response to terbutaline or 8-cpt cAMP stimulation. These data support the conclusion that β-adrenergic agonists produce acute activation of apical Cl− channels and that monolayers maintained under apical air interface conditions exhibit increased Na+ absorption.
The Journal of Membrane Biology – Springer Journals
Published: Jun 1, 2001
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