Culture of primary alveolar type II cells has been widely used to investigate the Na+ transport characteristics of alveolar epithelium. However, this model was restricted by early morphological and physiological dedifferentiation in culture. Recently, a cell line has been obtained by transfection of neonatal type II cells with the simian virus SV40 large T antigen gene (SV40‐T2). SV40‐T2 cells have retained proliferative characteristics of the primary type II cells (Clement et al., 1991, Exp. Cell Res., 196:198–205.) In the present study, we have characterized Na+ transport pathways in SV40‐T2 cells. SV40‐T2 cells retained most cardinal properties of the original alveolar epithelial cells. Na+ entry occurred, as in primary cultures, through both Na+‐cotransporters and amiloride‐sensitive Na+ channels. SV40‐T2 cells expressed Na+‐phosphate, Na+‐amino acid and Na+‐K+‐Cl− cotransports which are quantitatively similar to that of primary cultures. The existence of amiloride‐sensitive Na+ channels was supported by molecular and functional data. SV40‐T2 expressed the cloned α‐and γ‐mRNAs for the rat epithelial Na+ channel (rENaC), whereas β subunit was not detected, and 22Na+ influx was significantly inhibited by 10 μM amiloride. Na+, which enters SV40‐T2 cells, is extruded through a Na+, K+‐ATPase: mRNA for α1 and β1 isoforms of Na+, K+‐ATPase were present and Na+, K+‐ATPase activity was evidenced either on intact cells by the presence of a ouabain‐sensitive component of 86Rb+ influx or on cell homogenates by the measurement of ouabain‐inhibitable ATP hydrolysis. These results indicate that SV40‐T2 cell line displays most of the Na+ transport characteristics of well‐differentiated primary cells in the first days of culture. We conclude that the SV40‐T2 cell line provides a model of differentiated alveolar type II cells and may be a powerful tool to study, in vitro, the modulation of Na+ transport in pathophysiological conditions. © 1996 Wiley‐Liss, Inc.

To the Editor: Dipyridamole, a widely used vasodilatory drug, enhances renal tubular reabsorption of phosphate by decreasing adenosine uptake by tubular cells.1 In rats, dipyridamole prevents phosphate excretion induced by cyclic AMP and decreases the phosphaturic effect of parathyroid hormone.1 This demonstrates that adenosine, a local product of the degradation of nephrogenous cyclic AMP, is associated with phosphaturia. We sought to determine whether dipyridamole might decrease urinary phosphate excretion in humans. We evaluated the short-term effect of dipyridamole in 48 people (22 men and 26 women) with a mean age of 52 years (range, 26 to 74). Twelve were normal . . .