STIMULUS-SECRETION COUPLING IN PORCINE ADRENAL CHROMAFFIN CELLS - EFFECT OF DEXAMETHASONE

Recent studies from this laboratory established that dexamethasone (DE S) potentiates Ca2+ current via voltage-gated Ca2+ channels (VGCC), an d as a consequence potentiates agonist-induced cytosolic Ca2+ transien ts 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 mu M DEX significantly increased peak Ca 2+ current (Delta + 138%; n = 6; P < 0.05) in PAMC cells, DEX treatmen t also significantly potentiated the increase in cytosolic Ca2+ in res ponse to membrane depolarization with KCl (Delta + 20%; n = 29; P < 0. 05), but did not affect the amplitude of Ca2+ transients elicited by n icotine or acetylcholine. Despite the potentiation of intracellular Ca 2+, DEX treatment had no effect on KCl-induced secretion of either nor epinephrine or epinephrine, These data demonstrate that as in the rat chromaffin cell, DEX can also increase VGCC activity in PAMC cells. Ho wever, the subsequent potentiation of selected agonist-induced increas es in intracellular Ca2+ does not appear to be sufficient to alter cat echolamine secretion. (C) 1997 Wiley-Liss, Inc.