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

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.