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Lung epithelial fluid transport and the resolution of pulmonary edema

Journal

PHYSIOLOGICAL REVIEWS
Volume 82, Issue 3, Pages 569-600

Publisher

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/physrev.00003.2002

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Funding

  1. NHLBI NIH HHS [HL-51856, HL-51854] Funding Source: Medline

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The discovery of mechanisms that regulate salt and water transport by the alveolar and distal airway epithelium of the lung has generated new insights into the regulation of lung fluid balance under both normal and pathological conditions. There is convincing evidence that active sodium and chloride transporters are expressed in the distal lung epithelium and are responsible for the ability of the lung to remove alveolar fluid at the time of birth as well as in the mature lung when pathological conditions lead to the development of pulmonary edema. Currently, the best described molecular transporters are the epithelial sodium channel, the cystic fibrosis transmembrane conductance regulator, Na+-K+-ATPase, and several aquaporin water channels. Both catecholamine-dependent and -independent mechanisms can upregulate isosmolar fluid transport across the distal lung epithelium. Experimental and clinical studies have made it possible to examine the role of these transporters in the resolution of pulmonary edema.

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