Induction of calcium release from sarcoplasmic reticulum of skeletal muscle by xanthone and norathyriol

J. J. Kang, Y. W. Cheng, F. N. Ko, M. L. Kuo, C. N. Lin, C. M. Teng

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11 Citations (Scopus)

Abstract

1 Effects of xanthone and its derivative, 1,3,6,7-tetrahydroxyxanthone (norathyriol), on Ca2+ release and ryanodine binding were studied in isolated sarcoplasmic reticulum (SR) vesicles from rabbit skeletal muscle. 2 Both xanthone and norathyriol dose-dependently induced Ca2+ release from the actively loaded SR vesicles which was blocked by ruthenium red, a specific Ca2+ release inhibitor, and Mg2+. 3 Xanthone and norathyriol also dose-dependently increased apparent [3H]-ryanodine binding. Norathyriol, but not xanthone, produced a synergistic effect on binding activation when added concurrently with caffeine. 4 In the presence of Mg2+, which inhibits ryanodine binding, both caffeine and norathyriol, but not xanthone, could restore the binding to the level observed in the absence of Mg2+. 5 Xanthone activated the Ca2+-ATPase activity of isolated SR vesicles dose-dependently reaching 70% activation at 300 μM. 6 When tested in mouse diaphragm, norathyriol potentiated the muscle contraction followed by twitch depression and contracture in either a Ca2+-free bathing solution or one containing 2.5 mM Ca2+. These norathyriol-induced effects on muscle were inhibited by pretreatment with ruthenium red or ryanodine. 7 These data suggest that xanthone and norathyriol can induce Ca2+ release from the SR of skeletal muscle through a direct interaction with the Ca2+ release channel, also known as the ryanodine receptor.

Original languageEnglish
Pages (from-to)1736-1742
Number of pages7
JournalBritish Journal of Pharmacology
Volume118
Issue number7
Publication statusPublished - 1996
Externally publishedYes

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Keywords

  • Calcium release
  • Ryanodine receptor
  • Skeletal muscle
  • Xanthones

ASJC Scopus subject areas

  • Pharmacology

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