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

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

• Publisher: John Wiley and Sons
• Year: 1997
• Tongue: English
• Weight: 137 KB
• Volume: 49
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/(sici)1097-4547(19970815)49:4<416::aid-jnr3>3.0.co;2-b

✦ Synopsis

Recent studies from this laboratory established that dexamethasone (DEX) potentiates Ca 21 current via voltage-gated Ca 21 channels (VGCC), and as a consequence potentiates agonist-induced cytosolic Ca 21 transients in rat adrenal chromaffin cells. The present study examined whether DEX can also modulate VGCC activity and agonist-induced cytosolic Ca 21 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 mM DEX significantly increased peak Ca 21 current (D 1 138%; n 5 6; P F 0.05) in PAMC cells. DEX treatment also significantly potentiated the increase in cytosolic Ca 21 in response to membrane depolarization with KCl (D 1 20%; n 5 29; P F 0.05), but did not affect the amplitude of Ca 21 transients elicited by nicotine or acetylcholine. Despite the potentiation of intracellular Ca 21 , DEX treatment had no effect on KCl-induced secretion of either norepinephrine or epinephrine. These data demonstrate that as in the rat chromaffin cell, DEX can also increase VGCC activity in PAMC cells. However, the subsequent potentiation of selected agonist-induced increases in intracellular Ca 21 does not appear to be sufficient to alter catecholamine secretion.