Ca2+-activated K+ channels in airway smooth muscle are inhibited by cytoplasmic adenosine triphosphate

Klaus Groschner, Shai D. Silberberg, Craig H. Gelband, Cornelis van Breemen

Research output: Contribution to journalArticlepeer-review

27 Scopus citations

Abstract

Large-conductance Ca2+-activated K+ channels were studied in membranes of cultured rabbit airway smooth muscle cells, using the patch-clamp technique. In cell-attached recordings, channel openings were rare and occurred only at very positive potentials. Bradykinin (10 μM), an agonist which releases Ca2+ from the sarcoplasmic reticulum, transiently increased channel activity. The metabolic blocker 2,4-dinitrophenol (20 μM), which lowers cellular adenosine triphosphate (ATP) levels, induced a sustained increase of channel activity in cell-attached patches. In excised patches, these channels had a slope conductance of 155 pS at 0 mV, were activated by depolarization and by increasing the Ca2+ concentration at the cytoplasmic side above 10-7 mol/l. ATP, applied to the cytoplasmic side of the patches, dose-dependently decreased the channel's open-state probability. An inhibition constant (Ki) of 0.2 mmol/l was found for the ATP-induced inhibition. ATP reduced the Ca2+ sensitivity of the channel, shifting the Ca2+ activation curve to the right and additionally reducing its steepness. Our results demonstrate that cytoplasmic ATP inhibits a large-conductance Ca2+-activated K+ channel in airway smooth muscle. This ATP modulation of Ca2+-activated K+ channels might serve as an important mechanism linking energy status and the contractile state of the cells.

Original languageEnglish
Pages (from-to)517-522
Number of pages6
JournalPflugers Archiv European Journal of Physiology
Volume417
Issue number5
DOIs
StatePublished - 1 Jan 1991
Externally publishedYes

Keywords

  • ATP sensitivity
  • Airway smooth muscle
  • Ca-activated K channels
  • Patch-clamp

ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Physiology (medical)

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