AJP - Lung Cellular and Molecular Physiology, Vol 261, Issue 4 290-L295, Copyright © 1991 by American Physiological Society

ARTICLES

Potassium dependence of Na-Cl cotransport in dog tracheal epithelium

P. Fong, A. C. Chao and J. H. Widdicombe
Cystic Fibrosis Research Center, University of California, San Francisco 94143.

In confluent primary cultures of dog tracheal epithelium, we tested whether Cl entry across the basolateral membrane is by cotransport with K. Two approaches were taken. First, we measured the inhibition of short-circuit current (Isc) by the K channel inhibitor, Ba2+. Consistent with Na-K-2Cl cotransport, maximal doses of Ba2+ inhibited five-sixths of Isc in tissues previously stimulated to secrete Cl; only two-thirds of Isc should be sensitive to Ba2+ if NaCl cotransport is the entry mechanism. Second, we measured basolateral 86Rb uptake and demonstrated inhibition by bumetanide, an inhibitor of Na-K-2Cl cotransport in other tissues. The degree of inhibition by bumetanide was consistent with the levels of Cl secretion measured as Isc. Uptake of 86Rb was also reduced by removal of Na or Cl, and under these conditions Rb uptake was not further inhibited by bumetanide. These results suggest that the process responsible for Cl entry across the basolateral membrane of tracheal epithelium during Cl secretion is Na-K-2Cl rather than Na-Cl cotransport.

This article has been cited by other articles:

				J. H. Widdcombe How does cAMP increase active Na absorption across alveolar epithelium? Am J Physiol Lung Cell Mol Physiol, February 1, 2000; 278(2): L231 - L232. [Full Text] [PDF]