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EDITORIAL FOCUS

Store-operated Ca²⁺ entry in porcine airway smooth muscle

Departments of ¹Anesthesiology and ³Physiology & Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, Minnesota 55905; and ²Department of Anesthesiology, Marmara University, 34660 Istanbul, Turkey

Submitted 11 September 2003 ; accepted in final form 10 November 2003

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)-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 Ca²⁺ 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 IP₃ and RyR channels. Additional regulation of Ca²⁺ influx by agonist may be related to a receptor-operated, noncapacitative mechanism.

sarcoplasmic reticulum; calcium release-activated calcium channel; inositol trisphosphate; ryanodine; acetylcholine

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