Stimulus-secretion coupling in porcine adrenal chromaffin cells: Effect of dexamethasone

Lynn Z. Fuller, Chengbiao Lu, Douglas G. McMahon, Merlin D. Lindemann, Mark S. Jorgensen, Shane W. Rau, Jesse E. Sisken, Brian A. Jackson

Research output: Contribution to journalArticlepeer-review

17 Scopus citations


Recent studies from this laboratory established that dexamethasone (DEX) potentiates Ca2+ current via voltage-gated Ca2+ channels (VGCC), and as a consequence potentiates agonist-induced cytosolic Ca2+ transients in rat adrenal chromaffin cells. The present study examined whether DEX can also modulate VGCC activity and agonist-induced cytosolic Ca2+ transients in porcine adrenal medullary chromaffin (PAMC) cells, and if so whether this results in alterations in catecholamine secretion. Forty-eight-hr exposure to 1 μM DEX significantly increased peak Ca2+ current (Δ + 138%; n = 6; P < 0.05) in PAMC cells. DEX treatment also significantly potentiated the increase in cytosolic Ca2+ in response to membrane depolarization with KCl (Δ + 20%; n = 29; P < 0.05), but did not affect the amplitude of Ca2+ transients elicited by nicotine or acetylcholine. Despite the potentiation of intracellular Ca2+, DEX treatment had no effect on KCl-induced secretion of either norepinephrine or epinephrine. These data demonstrate that as in the rat chromafin cell, DEX can also increase VGCC activity in PAMC cells. However, the subsequent potentiation of selected agonist-induced increases in intracellular Ca2+ does not appear to be sufficient to alter catecholamine secretion.

Original languageEnglish
Pages (from-to)416-424
Number of pages9
JournalJournal of Neuroscience Research
Issue number4
StatePublished - Aug 15 1997


  • Adrenal medulla
  • Catecholamines
  • Chromaffin cell
  • Fura-2
  • Glucocorticoids
  • Intracellular calcium
  • Voltage-gated calcium channels

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience


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