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1 Departments of Physiology and Animal Science, University of Minnesota, St. Paul 55108; and 2 Department of Medicine, University of Minnesota, Minneapolis, Minnesota 55455
In this review, we discuss evidence that supports the
hypothesis that adrenergic stimulation of transepithelial Na absorption across the alveolar epithelium occurs indirectly by activation of
apical Cl channels, resulting in hyperpolarization and an increased driving force for Na uptake through amiloride-sensitive Na channels. This hypothesis differs from the prevailing idea that
adrenergic-receptor activation increases the open probability of
Na channels, leading to an increase in apical membrane Na
permeability and an increase in Na and fluid uptake from the alveolar
space. We review results from cultured alveolar epithelial cell
monolayer experiments that show increases in apical membrane Cl
conductance in the absence of any change in Na conductance after
stimulation by selective 
-adrenergic-receptor agonists. We also
discuss possible reasons for differences in Na-channel regulation in
cells grown in monolayer culture compared with that in dissociated
alveolar epithelial cells. Finally, we describe some preliminary in
vivo data that suggest a role for Cl-channel activation in the process
of amiloride-sensitive alveolar fluid absorption.
ion transport; epithelial sodium channel; cystic fibrosis transmembrane conductance regulator; terbutaline
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