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Am J Physiol Lung Cell Mol Physiol 297: L439-L454, 2009. First published June 19, 2009; doi:10.1152/ajplung.90268.2008
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UTP regulation of ion transport in alveolar epithelial cells involves distinct mechanisms

Chuanxiu Yang, Lijing Su, Yang Wang, and Lin Liu

Lundberg-Kienlen Lung Biology and Toxicology Laboratory, Department of Physiological Sciences, Oklahoma State University, Stillwater, Oklahoma

Submitted 8 April 2008 ; accepted in final form 4 June 2009

UTP is known to regulate alveolar fluid clearance. However, the relative contribution of alveolar type I cells and type II cells to this process is unknown. In this study, we investigated the effects of UTP on ion transport in type I-like cell (AEC I) and type II-like cell (AEC II) monolayers. Luminal treatment of cell monolayers with UTP increased short-circuit current (Isc) of AEC II but decreased Isc of AEC I. The Cl channel blockers NPPB and DIDS inhibited the UTP-induced changes in Isc ({Delta}Isc) in both types of cells. Amiloride, an inhibitor of epithelial Na+ channels (ENaC), abolished the UTP-induced {Delta}Isc in AEC I, but not in AEC II. The general blocker of K+ channels, BaCl2, eliminated the UTP-induced {Delta}Isc in AEC II, but not in AEC I. The intermediate conductance (IKCa) blocker, clofilium, also blocked the UTP effect in AEC II. The signal transduction pathways mediated by UTP were the same in AEC I and AEC II. Furthermore, UTP increased Cl secretion in AEC II and Cl absorption in AEC I. Our results suggest that UTP induces opposite changes in Isc in AEC I and AEC II, likely due to the reversed Cl flux and different contributions of ENaC and IKCa. Our results further imply a new concept that type II cells contribute to UTP-induced fluid secretion and type I cells contribute to UTP-induced fluid absorption in alveoli.

short-circuit current; fluid transport



Address for reprint requests and other correspondence: L. Liu, Dept. of Physiological Sciences, Oklahoma State Univ., 264 McElroy Hall, Stillwater, OK 74078 (e-mail: lin.liu{at}okstate.edu)







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