Expression and activity of epithelial sodium channel in hyperoxia‐induced bronchopulmonary dysplasia in neonatal rats

Abstract

The aim of the present study was to investigate the expression and activity of epithelial sodium channel (ENaC) in hyperoxia-induced bronchopulmonary dysplasia (BPD) in neonatal rats. Neonatal rats were exposed to hyperoxia to establish BPD models (control group was exposed to air), lung water was measured and Western blot was applied to detect the expression of three homologous subunits: α-, β- and γ-ENaC in the lung tissues. Furthermore, ATII cells were isolated from neonatal rats, and primarily cultured under normoxic or hyperoxic conditions. The ENaC expression was also examined in these cells. In addition, the amiloride-sensitive Na(+) currents induced by hyperoxia were recorded using the whole-cell patch clamp technique. The α-ENaC expression was increased after 5 days of hyperoxia in rat lung tissues, whereas not after 1, 3 and 7 days. ATII cells showed α-ENaC expression was reduced after 1 and 2 days' hyperoxia, but no change after 3 days. In contrast, β- and γ-ENaC expression was increased after hyperoxia in both in vivo and in vitro experiments. The amiloride-sensitive Na(+) currents in hyperoxia-exposed ATII cells were also increased, which was consistent with the upregulated expression of β- and γ-ENaC. Hyperoxia upregulates the expression of ENaC, especially β- and γ-ENaC subunits, in both neonatal rat lung tissues and ATII cells. Hyperoxia also enhanced the activity of ENaC in neonatal rat ATII cells. Dysfunctional transport of Na(+) may not be a key factor involving pulmonary edema at the early stage of BPD.