Amiloride-sensitive sodium channels and pulmonary edema.
Amiloride-sensitive sodium channels and pulmonary edema.
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DOI：
10.1155/2011/830320
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发表时间：
2011
影响因子：
4.3
通讯作者：
Fronius M
中科院分区：
文献类型：
--
作者：
Althaus M;Clauss WG;Fronius M
肺水肿的发生可被认为是由于液体过滤增加导致的肺泡灌流、肺泡-毛细血管屏障完整性受损以及由于肺泡液体清除率降低导致的消退障碍的组合。调节肺泡液体清除的重要机制是跨肺泡上皮的钠转运。跨上皮钠转运在很大程度上依赖于肺泡上皮细胞中钠通道的活性。本文介绍了在生理条件下，钠通道如何有助于肺泡液体清除，以及钠通道活性失调如何可能有助于肺水肿相关肺部疾病的发病机制。此外，钠通道作为假定的分子靶点治疗肺水肿进行了讨论。
The development of pulmonary edema can be considered as a combination of alveolar flooding via increased fluid filtration, impaired alveolar-capillary barrier integrity, and disturbed resolution due to decreased alveolar fluid clearance. An important mechanism regulating alveolar fluid clearance is sodium transport across the alveolar epithelium. Transepithelial sodium transport is largely dependent on the activity of sodium channels in alveolar epithelial cells. This paper describes how sodium channels contribute to alveolar fluid clearance under physiological conditions and how deregulation of sodium channel activity might contribute to the pathogenesis of lung diseases associated with pulmonary edema. Furthermore, sodium channels as putative molecular targets for the treatment of pulmonary edema are discussed.