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pubmed-article:10329950pubmed:abstractTextThe present study used real-time confocal microscopy to examine the effects of the beta2-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 alpha-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.lld:pubmed
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pubmed-article:10329950pubmed:dateRevised2009-11-19lld:pubmed
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pubmed-article:10329950pubmed:articleTitleEffect of beta-adrenoceptor activation on [Ca2+]i regulation in murine skeletal myotubes.lld:pubmed
pubmed-article:10329950pubmed:affiliationDepartments of Anesthesiology and of Physiology and Biophysics, Mayo Clinic and Foundation, Rochester 55905, Minnesota, USA.lld:pubmed
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pubmed-article:10329950pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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