DHEA attenuates catecholamine secretion from bovine adrenal chromaffin cells

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Abstract
Dehydroepiandrosterone (DHEA) is a putative anti-stress agent and stress is associated with the secretion of catecholamine from the adrenal gland, but the effects of DHEA on catecholamine secretion are not fully understood. Using bovine chromaffin cells, we found that DHEA inhibited catecholamine secretion and cytosolic Ca2+ ([Ca2+]i) rise coupled with nicotinic acetylcholine receptor (nAChR) without exerting an effect on3H-nicotine binding. In the case of high K+ stimulation, DHEA effectively suppressed secretion without affecting [Ca2+]1 rise. Trifluoperazine (TFP), a calmodulin inhibitor, was capable of counteracting the inhibition of DHEA on high K+-induced secretions. In permeabilized cells, DHEA suppressed the Ca2+-induced secretion. These results suggest that DHEA (a) acts as a channel blocker that suppresses Ca2+ influx and subsequent secretions associated with nAChR, or (b) affects the intracellular secretion machinery to suppress high K+-induced secretions without affecting the high K+-induced [Ca2+]i rise.