The Effect of Nicardipine on Capacitative Calcium Entry in Canine Pulmonary Arterial Smooth Muscle Cells

Abstract

Background: Capacitive calcium entry involves the influx of across the sarcolemma in response to the depletion of intracellular stores. Presently, little is known about the nature of the intracellular 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 . 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 stores and to monitor the development of the store-operated 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 leads to linear store-operated current (ISOC) reversal near 0 mV. Nicardipine does not affect ISOC. Conclusions: In canine PASMCs, the depletion of intracellular stores leads to the activation of ISOC, which is not inhibited by nicardipine, a voltage-dependent channel (VDCC) blocker, indicating that VDCC blocked by nicardipine does not contribute to CCE in canine PASMCs.