Capacitative Ca2+ entry in agonist-induced pulmonary vasoconstriction

Sharon S. McDaniel, Oleksandr Platoshyn, Jian Wang, Ying Yu, Michele Sweeney, Stefanie Krick, Lewis J. Rubin, Jason X.-J. Yuan
2001 American Journal of Physiology - Lung cellular and Molecular Physiology  
entry in agonist-induced pulmonary vasoconstriction. Am J Physiol Lung Cell Mol Physiol 280: L870-L880, 2001.-Agonist-induced increases in cytosolic Ca 2ϩ concentration ([Ca 2ϩ ]cyt) in pulmonary artery (PA) smooth muscle cells (SMCs) consist of a transient Ca 2ϩ release from intracellular stores followed by a sustained Ca 2ϩ influx. Depletion of intracellular Ca 2ϩ stores triggers capacitative Ca 2ϩ entry (CCE), which contributes to the sustained increase in [Ca 2ϩ ]cyt and the refilling of Ca
more » ... 2ϩ into the stores. In isolated PAs superfused with Ca 2ϩ -free solution, phenylephrine induced a transient contraction, apparently by a rise in [Ca 2ϩ ]cyt due to Ca 2ϩ release from the intracellular stores. The transient contraction lasted for 3-4 min until the Ca 2ϩ store was depleted. Restoration of extracellular Ca 2ϩ in the presence of phentolamine produced a contraction potentially due to a rise in [Ca 2ϩ ]cyt via CCE. The store-operated Ca 2ϩ channel blocker Ni 2ϩ reduced the store depletion-activated Ca 2ϩ currents, decreased CCE, and inhibited the CCE-mediated contraction. In single PASMCs, we identified, using RT-PCR, five transient receptor potential gene transcripts. These results suggest that CCE, potentially through transient receptor potential-encoded Ca 2ϩ channels, plays an important role in agonist-mediated PA contraction. transient receptor potential gene; pulmonary hypertension; pulmonary artery smooth muscle cells
doi:10.1152/ajplung.2001.280.5.l870 pmid:11290510 fatcat:3qpyspixx5czbgp2cxxcf5f3sm