Store-operated Ca2+ entry in porcine airway smooth muscle

Binnaz Ay, Y. S. Prakash, Christina M. Pabelick, Gary C. Sieck

Research output: Contribution to journalArticlepeer-review

93 Scopus citations


Ca2+ influx triggered by depletion of sarcoplasmic reticulum (SR) Ca2+ stores [mediated via store-operated Ca2+ channels (SOCC)] was characterized in enzymatically dissociated porcine airway smooth muscle (ASM) cells. When SR Ca2+ was depleted by either 5 μM cyclopiazonic acid or 5 mM caffeine in the absence of extracellular Ca2+, subsequent introduction of extracellular Ca2+ further elevated [Ca2+]i. SOCC was insensitive to 1 μM nifedipine- or KCl-induced changes in membrane potential. However, preexposure of cells to 100 nM-1 mM La3+ or Ni2+ inhibited SOCC. Exposure to ACh increased Ca2+ influx both in the presence and absence of a depleted SR. Inhibition of inositol 1,4,5-trisphosphate (IP 3)-induced SR Ca2+ release by 20 μM xestospongin D inhibited SOCC, whereas ACh-induced IP3 production by 5 μM U-73122 had no effect. Inhibition of Ca2+ release through ryanodine receptors (RyR) by 100 μM ryanodine also prevented Ca2+ influx via SOCC. Qualitatively similar characteristics of SOCC-mediated Ca 2+ influx were observed with cyclopiazonic acid- vs. caffeine-induced SR Ca2+ depletion. These data demonstrate that a Ni2+/La3+-sensitive Ca2+ influx via SOCC in porcine ASM cells involves SR Ca2+ release through both IP 3 and RyR channels. Additional regulation of Ca2+ influx by agonist may be related to a receptor-operated, noncapacitative mechanism.

Original languageEnglish (US)
Pages (from-to)L909-L917
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number5 30-5
StatePublished - May 2004


  • Acetylcholine
  • Calcium release-activated calcium channel
  • Inositol trisphosphate
  • Ryanodine
  • Sarcoplasmic reticulum

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology


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