Functions of aquaporin 1 and α-epithelial Na+ channel in rat acute lung injury induced by acute ischemic kidney injury

Abstract

To establish a rat model of acute ischemic kidney injury by continually occluding the bilateral renal artery and renal veins, the functions of α-epithelial Na(+) channel (α-ENaC) and aquaporin (AQP1) in lung injury induced by acute kidney injury (AKI) were examined and compared with lung injury induced by endotoxin. Male Wistar rats were randomly divided into three groups: control group, AKI group, and sepsis group. The concentrations of AQP1 and α-ENaC in the lung tissue were detected. The concentrations of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in the serum and bronchoalveolar lavage fluid were also detected. The arterial blood pH in AKI group and PaO2 in sepsis group decreased 2 h after the experiment. A significant pulmonary interstitial and alveolar space edema, which showed a typical pathological change in acute lung injury, was found in AKI and sepsis group 8 h after the experiment. Two hours after the experiment, the concentration of TNF-α and IL-6 in the serum and bronchoalveolar lavage fluid (BALF) in AKI and sepsis group increased, whereas the pulmonary expression of AQP1 and α-ENaC decreased. The pulmonary AQP1 and α-ENaC of the rats were negatively correlated with TNF-α and IL-6 in BALF. The relevance among AQP1, α-ENaC, TNF-α, and IL-6 in sepsis group was higher than that in AKI group. The TNF-α and IL-6 levels increased significantly and the pulmonary expression of AQP1 and α-ENaC declined at the early stage of AKI.