Stimulus-secretion coupling in porcine adrenal chromaffin cells: Acute effects of glucocorticoids

✍ Scribed by Paul G. Wagner; Mark S. Jorgensen; Warwick A. Arden; Brian A. Jackson

• Publisher: John Wiley and Sons
• Year: 1999
• Tongue: English
• Weight: 125 KB
• Volume: 57
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/(sici)1097-4547(19990901)57:5<643::aid-jnr6>3.0.co;2-e

✦ Synopsis

Recent studies from this laboratory have established that long-term exposure (48 hr) to glucocorticoids can modulate voltage-gated Ca 2؉ channel activity and subsequent intracellular Ca 2؉ transients in porcine adrenal medullary chromaffin (PAMC) cells maintained in primary culture. Consistent with many steroid hormone-mediated responses, this chronic effect of glucocorticoids probably involves increased gene expression and protein synthesis. However, there is now considerable evidence to suggest that steroids can also elicit acute, non-genomic effects. The aim of the present study was to determine whether acute exposure to glucocorticoids also affects nicotinic receptor-dependent catecholamine (CAT) secretion and Ca 2؉ signaling in PAMC cells. Acute exposure to dexamethasone (DEX) dose-dependently attenuated the degree of nicotine (NIC)-induced CAT secretion, as well as the amplitude of NIC-induced intracellular Ca 2؉ transients. Significant inhibition of CAT secretion occurred immediately upon addition of DEX, reached maximal levels within 5 min of exposure to DEX, and was rapidly reversible after steroid washout. The endogenous porcine glucocorticoid cortisol elicited similar effects. In contrast, DEX had no significant effect on KCl-induced CAT secretion or intracellular Ca 2؉ transients. These data demonstrate that acute exposure to glucocorticoids can modulate stimulus-secretion coupling in PAMC cells and suggest that the primary site of action is the nicotinic receptor. J.