ABSTRACT
BACKGORUND: Capacitive calcium entry involves the influx of Ca2+ across the sarcolemma in response to the depletion of intracellular Ca2+ stores. Presently, little is known about the nature of the intracellular Ca2+ store (s) in pulmonary arterial smooth muscle cells (PASMCs), even though the unique contractile response of this tissue to hypoxia may at least partially involve the intracellular release of Ca2+ . The authors aimed to investigate the effects of nicardipine on capacitative calcium entry. METHODS: isolated pulmonary smooth muscle cells were obtained from enzymatically treated canine pulmonary artery. Currents were recorded at room temperature using the dialyzed whole cell recording technique. The protocol used to deplete intracellular Ca2+ stores and to monitor the development of the store-operated Ca2+ currents, involved cells being were voltage-clamped at 0 mv to inactivate any voltage-dependent calcium currents, which were recorded in response to a 200 ms voltage step from 120 to 40 mV in 20 mV increments. RESULTS: Simultaneous depletion of intracellular Ca2+ leads to linear store-operated Ca2+ current (iSOC) reversal near 0 mV. Nicardipine does not affect iSOC. CONCLUSiONS: in canine PASMCs, the depletion of intracellular Ca2+ stores leads to the activation of iSOC, which is not inhibited by nicardipine, a voltage-dependent Ca2+ channel (VDCC) blocker, indicating that VDCC blocked by nicardipine does not contribute to CCE in canine PASMCs.