Abstract
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 language | English (US) |
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Pages (from-to) | C1038-C1045 |
Journal | American Journal of Physiology - Cell Physiology |
Volume | 276 |
Issue number | 5 45-5 |
DOIs | |
State | Published - 1999 |
Keywords
- Adenosine 3',5'-cyclic monophosphate
- Ryanodine receptor
- Sarcoplasmic reticulum
- Skeletal muscle
ASJC Scopus subject areas
- Physiology
- Cell Biology