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This Article Full Text Full Text (PDF) All Versions of this Article: 293/5/L1332    most recent 00338.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Güney, S. Articles by Mairbäurl, H. Search for Related Content PubMed PubMed Citation Articles by Güney, S. Articles by Mairbäurl, H.

Dexamethasone prevents transport inhibition by hypoxia in rat lung and alveolar epithelial cells by stimulating activity and expression of Na⁺-K⁺-ATPase and epithelial Na⁺ channels

evin Güney,^2,* Akelei Schuler,^1,* Alexandra Ott,^1,* Sabine Höschele,¹ Stefanie Zügel,¹ Emel Balolu,¹ Peter Bärtsch,¹ and Heimo Mairbäurl¹

¹Medical Clinic VII, Sports Medicine, University Hospital Heidelberg, University of Heidelberg, Heidelberg, Germany; and ²Department of Physiology, Gazi University School of Medicine, Ankara, Turkey

Submitted 31 August 2006 ; accepted in final form 11 September 2007

Hypoxia inhibits Na and lung fluid reabsorption, which contributes to the formation of pulmonary edema. We tested whether dexamethasone prevents hypoxia-induced inhibition of reabsorption by stimulation of alveolar Na transport. Fluid reabsorption, transport activity, and expression of Na transporters were measured in hypoxia-exposed rats and in primary alveolar type II (ATII) cells. Rats were treated with dexamethasone (DEX; 2 mg/kg) on 3 consecutive days and exposed to 10% O₂ on the 2nd and 3rd day of treatment to measure hypoxia effects on reabsorption of fluid instilled into lungs. ATII cells were treated with DEX (1 µM) for 3 days before exposure to hypoxia (1.5% O₂). In normoxic rats, DEX induced a twofold increase in alveolar fluid clearance. Hypoxia decreased reabsorption (–30%) by decreasing its amiloride-sensitive component; pretreatment with DEX prevented the hypoxia-induced inhibition. DEX increased short-circuit currents (ISC) of ATII monolayers in normoxia and blunted hypoxic transport inhibition by increasing the capacity of Na⁺-K⁺-ATPase and epithelial Na⁺ channels (ENaC) and amiloride-sensitive ISC. DEX slightly increased the mRNA of - and -ENaC in whole rat lung. In ATII cells from DEX-treated rats, mRNA of ₁-Na⁺-K⁺-ATPase and -ENaC increased in normoxia and hypoxia, and -ENaC was increased in normoxia only. DEX stimulated the mRNA expression of ₁-Na⁺-K⁺-ATPase and -, -, and -ENaC of A549 cells in normoxia and hypoxia (1.5% O₂) when DEX treatment was begun before or during hypoxic exposure. These results indicate that DEX prevents inhibition of alveolar reabsorption by hypoxia and stimulates the expression of Na transporters even when it is applied in hypoxia.

hypoxic pulmonary edema; alveolar fluid reabsorption; mRNA expression; ion transport

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