Muscarinic receptor stimulation modulates the effect of halothane on Mn2+ influx in airway smooth muscle

David O. Warner, Keith A. Jones, Robert R. Lorenz, Christina M. Pabelick

Research output: Contribution to journalArticle

6 Scopus citations

Abstract

Prior studies suggest that the mechanism of action by which halothane relaxes airway smooth muscle depends on the contractile state of the cell. We hypothesized that halothane would inhibit the influx of Ca2+ into canine airway smooth muscle cells during submaximal, but not maximal, muscarinic stimulation. This hypothesis was tested by using the rate of quenching of fura 2 fluorescence by Mn2+ in strips of canine tracheal smooth muscle as an index of Ca2+ influx. Acetylcholine (ACh) produced a dose-dependent increase in Mn2+ influx. Halothane (0.64 ± 0.05 mM) significantly decreased Mn2+ influx and intracellular Ca2+ concentration when added to strips stimulated with a submaximal concentration of ACh (0.3 μM) but had no effect on Mn2+ influx or intracellular Ca2+ concentration during maximal stimulation with ACh (100 μM). Similar results were observed when the strips were treated with verapamil. These results demonstrate that anesthetic effects on Ca2+ homeostasis in intact canine tracheal smooth muscle cells may be critically modulated by receptor-linked mechanisms.

Original languageEnglish (US)
Pages (from-to)C868-C873
JournalAmerican Journal of Physiology - Cell Physiology
Volume273
Issue number3 42-3
DOIs
StatePublished - Sep 1997

Keywords

  • Anesthesia
  • Calcium channels
  • Calcium influx
  • Lung
  • Volatile anesthetics

ASJC Scopus subject areas

  • Physiology
  • Cell Biology

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