Calcium inflow in cells transfected with cloned rat and porcine calcitonin receptors

David M. Findlay, Souheir Houssami, Patrick M. Sexton, Catherine L. Brady, T. John Martin, Damian E. Myers

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Ca 2+ fluxes were examined in HEK 293 cells stably expressing the rat or porcine calcitonin receptors (CTRs). Calcitonin (CT) rapidly increased cytosolic Ca 2+ ([Ca 2+ ] i ) concentrations in these cells in a manner which was sustained in the presence of extracellular Ca 2+ ([Ca 2+] e ). In cells pretreated with CT, elevation of the [Ca 2+ ] e concentration resulted in a further increase in [Ca 2+ ] i which was concentration-dependent with respect to both the concentration of CT and the increment of [Ca 2+ e . Untransfected cells, cells transfected with vector alone, and CTR-transfected cells not treated with CT, were unresponsive to [Ca 2+ ] e . The microsomal Ca 2+ -ATPase inhibitor thapsigargin was able to mimic both the acute [Ca 2+ ] i fluxes and responsiveness to [Ca 2+ ] e mediated by Cr in these cells. The CT-induced responsiveness to [Ca 2+ ] e was neither mimicked by, nor affected by, activators of the cAMP or protein kinase C pathways. Treatment of cells with pertussis toxin influenced neither the primary Ca 2+ fluxes in response to CT or thapsigargin nor the agonist-induced [Ca 2+ ] e influx. Nifedipine failed to block responses to either CT or thapsigargin. These results lead to the important conclusion that the CTR participates in receptor-activated Ca 2+ inflow, in which depletion of intracellular Ca 2+ pools leads secondarily to influx of extracellular Ca2+.

Original languageEnglish
Pages (from-to)213-219
Number of pages7
JournalBBA - Molecular Cell Research
Issue number2-3
Publication statusPublished - 16 Mar 1995
Externally publishedYes


  • Calcium influx
  • Cloned calcitonin receptor
  • Thapsigargin
  • Transfected HEK 293 cell

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