Hypoxia reversibly inhibits epithelial sodium transport but does not inhibit lung ENaC or Na-K-ATPase expression
Hypoxia reversibly inhibits epithelial sodium transport but does not inhibit lung ENaC or Na-K-ATPase expression
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DOI：
10.1152/ajplung.00181.2002
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发表时间：
2003-01-01
影响因子：
4.9
通讯作者：
Weil, JV
中科院分区：
文献类型：
--
作者：
Carpenter, TC;Schomberg, S;Weil, JV
低氧可降低肺泡液体清除量和鼻电位差，后者是呼吸道上皮钠转运的标志。这种体内上皮钠转运受损的机制仍不确定。我们假设，低氧损伤的上皮钠转运会随着复氧而迅速恢复，低氧会降低肺上皮钠通道和Na，K-ATPase的表达。我们研究了成年大鼠暴露在常氧、低氧(FiO2=0.1)24小时或低氧后在常氧中恢复的情况。鼻电位差在低氧时降低了40%(P<；0.001)，在复氧后恢复到基线水平。肺Na，K-ATPase活性在低氧状态下下降40%(P=0.003)，在复氧状态下恢复到基础水平。肺上皮钠通道-α，--β、-γ和Na，K-α(1)基因的表达在低氧或复氧后无明显变化，ENaC-α、ENaC-β、Na，K-ATPase-α(1)和Na，K-ATPase-β(1)蛋白的表达也无明显变化。我们的结论是，亚急性暴露于中度低氧可逆转地损害呼吸道上皮钠转运和肺Na，K-ATPase活性，但这些变化不是由于肺钠转运蛋白表达的变化。
Hypoxia reduces alveolar liquid clearance and the nasal potential difference, a marker of airway epithelial sodium transport. The mechanisms underlying this impaired epithelial sodium transport in vivo remain uncertain. We hypothesized that epithelial sodium transport impaired by hypoxia would recover quickly with reoxygenation and that hypoxia decreases the expression of lung epithelial sodium channels and Na, K-ATPases. We studied adult rats exposed to normoxia, hypoxia (FIO2 = 0.1) for 24 h, or hypoxia followed by recovery in normoxia. Nasal potential differences decreased by 40% with hypoxia (P < 0.001), returning to baseline levels with reoxygenation. Lung Na, K-ATPase activity decreased by 40% with hypoxia (P = 0.003), recovering to baseline levels with reoxygenation. Lung expression of mRNA encoding for epithelial sodium channel (ENaC)-α,- -β, and -γ or for Na, K-ATPase-α(1) did not change significantly with hypoxia or recovery nor did lung expression of ENaC-α, ENaC-β, Na, K-ATPase-α(1), or Na, K-ATPase-β(1) protein. We conclude that subacute exposure to moderate hypoxia reversibly impairs airway epithelial sodium transport and lung Na, K-ATPase activity but that those changes are not due to changes in the lung expression of sodium-transporting proteins.