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Postnatal glucocorticoids induce -ENaC formation and regulate glucocorticoid receptors in the preterm rabbit lung

¹Department of Pediatrics/Division of Neonatology, University of Texas Health Science Center, San Antonio, 78229-3900; ²Wilford Hall United States Air Force Medical Center, San Antonio 78236; ³Department of Pediatrics, University of Texas-Houston Medical School, Houston, Texas 77030

Submitted 15 October 2002 ; accepted in final form 26 August 2003

At birth, lung fluid clearance is coupled to Na⁺ transport through epithelial Na⁺ channels (ENaC) in the distal lung epithelium. We evaluated the effect of postnatal glucocorticoids (GC) on lung -ENaC expression in preterm 29-day gestational age (GA) fetal rabbits. Postnatal treatment of 29-day GA fetuses with 0.5 mg/kg of dexamethasone (Dex) iv resulted in a 2- and 22-fold increase in lung -ENaC mRNA expression compared with saline-treated fetuses after 8 and 16 h, respectively. Lung -ENaC protein levels in Dex-treated fetuses were also elevated compared with saline-treated counterparts. The extravascular lung water (EVLW)/dry lung tissue weight ratios of 29-day GA fetuses treated with either saline or Dex decreased over 24 h compared with that observed at birth; however, at 24 h, the EVLW/dry lung tissue weight ratios of saline- and Dex-treated fetuses were similar. Dex-induced -ENaC mRNA and protein levels were attenuated by glucocorticoid receptor (GCR) antagonist RU-486 in fetal distal lung epithelial cells isolated from 29-day GA fetuses, indicating that GC-dependent augmentation of lung -ENaC requires the presence of functional GCR. Lung GCR mRNA expression and protein levels were elevated in 29-day GA fetuses compared with fetuses at earlier GA. Exposure of 29-day GA fetuses to Dex for 16 h caused a 2.1-fold increase in lung GCR mRNA expression, but GCR protein levels were decreased in Dex-treated fetuses after 24 h. We conclude that postnatal treatment of preterm 29-day GA fetal rabbits with GC results in an elevation of lung -ENaC accompanied by an autoregulation of pulmonary GCR.

epithelial sodium channels; respiratory distress syndrome

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