Effect of β-adrenoceptor activation on [Ca2+](i) regulation in murine skeletal myotubes

Y. S. Prakash, H. F.M. Van Der Heijden, E. M. Gallant, G. C. Sieck

Research output: Contribution to journalArticlepeer-review

18 Scopus citations


The present study used real-time confocal microscopy to examine the effects of the β2-adrenoceptor agonist salbutamol on regulation of intracellular Ca2+ concentration ([Ca2+](i)) in myotubes derived from neonatal mouse limb muscles. Immunocytochemical staining for ryanodine receptors and skeletal muscle myosin confirmed the presence of sarcomeres. The myotubes displayed both spontaneous and ACh-induced rapid (<2-ms rise time) [Ca2+](i) transients. The [Ca2+](i) transients were frequency modulated by both low and high concentrations of salbutamol. Exposure to α- bungarotoxin and tetrodotoxin inhibited ACh-induced [Ca2+](i) transients and the response to low concentrations of salbutamol but not the response to higher concentrations. Preexposure to caffeine inhibited the subsequent [Ca2+](i) response to lower concentrations of salbutamol and significantly blunted the response to higher concentrations. Preexposure to salbutamol diminished the [Ca2+](i) response to caffeine. Inhibition of dihydropyridine-sensitive Ca2+ channels with nifedipine or PN-200-110 did not prevent [Ca2+](i) elevations induced by higher concentrations of salbutamol. The effects of salbutamol were mimicked by the membrane-permeant analog dibutyryl adenosine 3',5'-cyclic monophosphate. These data indicate that salbutamol effects in skeletal muscle predominantly involve enhanced sarcoplasmic reticulum Ca2+ release.

Original languageEnglish (US)
Pages (from-to)C1038-C1045
JournalAmerican Journal of Physiology - Cell Physiology
Issue number5 45-5
StatePublished - 1999


  • Adenosine 3',5'-cyclic monophosphate
  • Ryanodine receptor
  • Sarcoplasmic reticulum
  • Skeletal muscle

ASJC Scopus subject areas

  • Physiology
  • Cell Biology


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