This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Matalon, S. Articles by Davis, I. C. Search for Related Content PubMed PubMed Citation Articles by Matalon, S. Articles by Davis, I. C. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB OUABAIN SODIUM Related Collections Ion channels/membrane transport Pulmonary biology and circulation

(Circulation Research. 2003;92:348.)
© 2003 American Heart Association, Inc.

Editorials

Vectorial Sodium Transport Across the Mammalian Alveolar Epithelium

It Occurs but Through Which Cells?

Sadis Matalon, Ian C. Davis

From the Department of Anesthesiology, University of Alabama at Birmingham, Birmingham, Ala.

Correspondence to Sadis Matalon, PhD, Alice McNeal Professor of Anesthesiology, University of Alabama at Birmingham, UAB Dept of Anesthesiology, 1530 3rd Ave South, Birmingham, AL 35294-2172. E-mail sadis.matalon@ccc.uab.edu

Key Words: alveolar type I/II cells • Na⁺,K⁺-ATPase isoforms • sodium channels • alveolar fluid clearance • pulmonary edema

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The fluid that fills the alveolar spaces in the fetal lung is cleared shortly after birth, mainly as a consequence of active transport of sodium ions (Na⁺) across the alveolar epithelium. This transport establishes an osmotic gradient that favors reabsorption of intra-alveolar fluid.¹ Studies that demonstrate both the reabsorption of intratracheally instilled isotonic fluid or plasma from the alveolar spaces of adult anesthetized animals and resected human lungs, and the partial inhibition of this process by amiloride and ouabain, indicate that adult alveolar epithelial cells are also capable of actively transporting Na⁺ ions (see reviews^2,3). Although it remains unclear whether active Na⁺ transport plays an important role in keeping alveolar spaces free of fluid in the normal lung, a variety of studies have clearly established that active Na⁺ transport limits the degree of alveolar edema under pathological conditions in which the alveolar epithelium has been damaged. For example, intratracheal instillation of a Na⁺ channel blocker in rats exposed to hyperoxia increased the amount of extravascular lung water.⁴ Conversely, intratracheal instillation of adenoviral vectors expressing the Na⁺,K⁺-ATPase genes increased survival of rats exposed to hyperoxia.⁵ Moreover, patients with acute lung injury who are still able to concentrate alveolar protein (as a result of active Na⁺ reabsorption) have a better prognosis than those who cannot.^6,7

Insight into the nature and regulation of transport pathways has come from electrophysiological studies of freshly isolated and cultured alveolar type II (ATII) cells. These cells, which make up 67% of the alveolar . . . [Full Text of this Article]

This article has been cited by other articles:

				Y. Berthiaume Long-term stimulation of alveolar epithelial cells by {beta}-adrenergic agonists: increased Na+ transport and modulation of cell growth? Am J Physiol Lung Cell Mol Physiol, October 1, 2003; 285(4): L798 - L801. [Full Text] [PDF]