Inhibition of Na+-K+-ATPase activates Na+-K+-2Cl- cotransporter activity in cultured ciliary epithelium

J. Dong, N. A. Delamere, M. Coca-Prados

Research output: Contribution to journalArticle

26 Scopus citations

Abstract

86Rb uptake experiments were conducted to measure Na+-K+-ATPase activity and Na+-K+-2Cl- cotransporter activity in a cell line derived from rabbit nonpigmented ciliary epithelium. The presence of a Na+-K+- 2Cl- cotransporter was supported by the observation of a bumetanide- sensitive 86Rb uptake component that was dependent on the extracellular concentration of both sodium and chloride. Potassium influx mediated by the Na+-K+-2Cl- cotransporter and Na+-K+-ATPase accounted for ~46 and 33% of total potassium uptake, respectively, whereas both ouabain- and bumetanide-resistent uptake accounted for 9%. Inhibition of the Na+-K+- ATPase had a stimulatory effect on Na+-K+-2Cl- cotransporter activity, which was dependent on the extent and duration of Na+-K+-ATPase inhibition. Ouabain treatment stimulated the potassium (86Rb) efflux rate and reduced intracellular potassium ([K](i)). Potassium channel blockers suppressed the ouabain-activated potassium efflux and inhibited the ouabain-induced activation of the Na+-K+-2Cl- cotransporter. We conclude that Na--K+- ATPase inhibition leads to the opening of potassium channels, which exacerbates the depletion of cellular potassium; Na+-K+-2Cl- cotransporter stimulation caused by the fall of [K](i) overrides the tendency of increased cellular sodium to inhibit the cotransporter.

Original languageEnglish (US)
Pages (from-to)C198-C205
JournalAmerican Journal of Physiology - Cell Physiology
Volume266
Issue number1 35-1
StatePublished - Jan 1 1994
Externally publishedYes

Keywords

  • ciliary epithelium
  • potassium channel
  • sodium-potassium adenosinetriphosphatase
  • sodium-potassium-two chloride cotransporter

ASJC Scopus subject areas

  • Physiology
  • Cell Biology

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