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1 Medical Clinic and Polyclinic, Department of Internal Medicine VII, Sports Medicine, University of Heidelberg, 69115 Heidelberg, Germany; and 2 Will Rogers Institute Pulmonary Research Center, Department of Medicine, University of Southern California, Los Angeles, California 90033
L665, 2002. First published December 14, 2001; 10.1152/ajplung.00355.2001.
Hypoxia has been reported to inhibit
activity and expression of ion transporters of alveolar epithelial
cells. This study extended those observations by investigating the
mechanisms underlying inhibition of active Na transport across primary
cultured adult rat alveolar epithelial cell monolayers grown on
polycarbonate filters. Cell monolayers were exposed to normoxia and
hypoxia (1.5% and 5% O2, 5% CO2), and
resultant changes in bioelectric properties [i.e., short-circuit
current (Isc) and transepithelial resistance
(Rt)] were measured in Ussing chambers. Results
showed that Isc decreased with duration of
exposure to hypoxia, while relatively little change was observed for
Rt. In normoxia, amiloride inhibited ~70% of
Isc. The amiloride-sensitive portion of
Isc decreased over time of exposure to hypoxia,
whereas the magnitude of the amiloride-insensitive portion of
Isc was not affected. Na pump capacity measured
after permeabilization of the apical plasma membrane with amphotericin
B decreased in monolayers exposed to 1.5% O2 for 24 h, as did the capacity of amiloride-sensitive Na uptake measured after
imposing an apical to basolateral Na gradient and permeabilization of
the basolateral membrane. These results demonstrate that exposure to
hypoxia inhibits alveolar epithelial Na reabsorption by reducing the
rates of both apical amiloride-sensitive Na entry and basolateral Na extrusion.
alveolar type II cells; Ussing chambers; sodium channels; sodium pump; amphotericin B
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