Potassium dependence of Na-Cl cotransport in dog tracheal epithelium

P. Fong, A. C. Chao, Jonathan Widdicombe

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

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 (I(sc)) by the K channel inhibitor, Ba2+. Consistent with Na-K-2Cl cotransport, maximal doses of Ba2+ inhibited five-sixths of I(sc) in tissues previously stimulated to secrete Cl; only two-thirds of I(sc) 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 I(sc). 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.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume261
Issue number4 5-2
StatePublished - 1991
Externally publishedYes

Fingerprint

Bumetanide
Potassium
Epithelium
Dogs
Membranes

Keywords

  • barium ion
  • bumetanide
  • sodium-potassium-2-chloride cotransport

ASJC Scopus subject areas

  • Cell Biology
  • Physiology
  • Pulmonary and Respiratory Medicine

Cite this

Potassium dependence of Na-Cl cotransport in dog tracheal epithelium. / Fong, P.; Chao, A. C.; Widdicombe, Jonathan.

In: American Journal of Physiology - Lung Cellular and Molecular Physiology, Vol. 261, No. 4 5-2, 1991.

Research output: Contribution to journalArticle

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