Halothane and potassium channels in airway smooth muscle

T. Fukushima, A. Hirasaki, K. A. Jones, David Oman Warner

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Earlier studies have suggested that halothane may relax smooth muscle in part by opening adenosine triphosphate-sensitive potassium (K(ATP)) channels. We tested this hypothesis in vitro by examining the interaction of halothane with glibenclamide, a K(ATP) channel blocker, and YM934, a K(ATP) channel opener, in strips of canine tracheal smooth muscles mounted in an organ bath system. To examine the specificity of any effects of halothane on the K(ATP) channel, we assessed the interaction of halothane with tetraethylammonium (TEA), an antagonist of the large-conductance, calcium-activated potassium channel. Experiments were conducted with drugs added before exposure to increasing concentrations of acetylcholine (ACh), and with drugs added after stable increases in force produced by ACh were achieved (ACh precontraction). Exposure to halothane 0.62 mmol litre -1 (equivalent to approximately 2 MAC) increased significantly the ED 50 for ACh-induced contractions (by 0.24 (SEM 0.07) μmol litre -1). TEA 1 mmol litre -1 but not glibenclamide 10 μmol litre -1 significantly augmented this increase in ED 50 (by an additional 0.17 (0.06) μmol litre -1). In strips precontracted with ACh, TEA, but not glibenclamide, potentiated concentration-dependent relaxation induced by halothane. Incubation with YM934 0.32 μmol litre -1 increased significantly the ED 50 for ACh-induced contractions (from 0.12 (0.02) to 0.55 (0.11) μmol litre -1), an increase not affected by exposure to halothane 0.72 mmol litre -1. When added to strips precontracted with approximately ACh 0.3 μmol litre -1, YM934 produced concentration-dependent relaxation; halothane had little effect on this relaxation. These results do not support the hypothesis that halothane relaxes canine tracheal smooth muscle in part by opening K(ATP) channels.

Original languageEnglish (US)
Pages (from-to)847-853
Number of pages7
JournalBritish Journal of Anaesthesia
Volume76
Issue number6
StatePublished - 1996

Fingerprint

Potassium Channels
Halothane
Smooth Muscle
Acetylcholine
Adenosine Triphosphate
Tetraethylammonium
Glyburide
Canidae
Potassium Channel Blockers
Large-Conductance Calcium-Activated Potassium Channels
Baths
Pharmaceutical Preparations

Keywords

  • Airway, muscles
  • Anaesthetics volatile, halothane
  • Ions, ion channels
  • Ions, potassium
  • Lung, trachea

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Fukushima, T., Hirasaki, A., Jones, K. A., & Warner, D. O. (1996). Halothane and potassium channels in airway smooth muscle. British Journal of Anaesthesia, 76(6), 847-853.

Halothane and potassium channels in airway smooth muscle. / Fukushima, T.; Hirasaki, A.; Jones, K. A.; Warner, David Oman.

In: British Journal of Anaesthesia, Vol. 76, No. 6, 1996, p. 847-853.

Research output: Contribution to journalArticle

Fukushima, T, Hirasaki, A, Jones, KA & Warner, DO 1996, 'Halothane and potassium channels in airway smooth muscle', British Journal of Anaesthesia, vol. 76, no. 6, pp. 847-853.
Fukushima, T. ; Hirasaki, A. ; Jones, K. A. ; Warner, David Oman. / Halothane and potassium channels in airway smooth muscle. In: British Journal of Anaesthesia. 1996 ; Vol. 76, No. 6. pp. 847-853.
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AB - Earlier studies have suggested that halothane may relax smooth muscle in part by opening adenosine triphosphate-sensitive potassium (K(ATP)) channels. We tested this hypothesis in vitro by examining the interaction of halothane with glibenclamide, a K(ATP) channel blocker, and YM934, a K(ATP) channel opener, in strips of canine tracheal smooth muscles mounted in an organ bath system. To examine the specificity of any effects of halothane on the K(ATP) channel, we assessed the interaction of halothane with tetraethylammonium (TEA), an antagonist of the large-conductance, calcium-activated potassium channel. Experiments were conducted with drugs added before exposure to increasing concentrations of acetylcholine (ACh), and with drugs added after stable increases in force produced by ACh were achieved (ACh precontraction). Exposure to halothane 0.62 mmol litre -1 (equivalent to approximately 2 MAC) increased significantly the ED 50 for ACh-induced contractions (by 0.24 (SEM 0.07) μmol litre -1). TEA 1 mmol litre -1 but not glibenclamide 10 μmol litre -1 significantly augmented this increase in ED 50 (by an additional 0.17 (0.06) μmol litre -1). In strips precontracted with ACh, TEA, but not glibenclamide, potentiated concentration-dependent relaxation induced by halothane. Incubation with YM934 0.32 μmol litre -1 increased significantly the ED 50 for ACh-induced contractions (from 0.12 (0.02) to 0.55 (0.11) μmol litre -1), an increase not affected by exposure to halothane 0.72 mmol litre -1. When added to strips precontracted with approximately ACh 0.3 μmol litre -1, YM934 produced concentration-dependent relaxation; halothane had little effect on this relaxation. These results do not support the hypothesis that halothane relaxes canine tracheal smooth muscle in part by opening K(ATP) channels.

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