Vectorial sodium transport across the mammalian alveolar epithelium: it occurs but through which cells?

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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 reviews2,3). 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 epithelial cell population, but which constitute only 3% of the alveolar surface area in the adult lung, can be isolated at high purity and cultured …