DHEA attenuates catecholamine secretion from bovine adrenal chromaffin cells.

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 Ca(2+) ([Ca(2+)](i)) rise coupled with nicotinic acetylcholine receptor (nAChR) without exerting an effect on (3)H-nicotine binding. In the case of high K(+) stimulation, DHEA effectively suppressed secretion without affecting [Ca(2+)](i) 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 Ca(2+)-induced secretion. These results suggest that DHEA (a) acts as a channel blocker that suppresses Ca(2+) 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 [Ca(2+)](i) rise.

journal_name

J Biomed Sci

authors

Liu PS,Wang PY

doi

10.1007/BF02256563

keywords:

subject

Has Abstract

pub_date

2004-03-01 00:00:00

pages

200-5

issue

2

eissn

1021-7770

issn

1423-0127

pii

76032

journal_volume

11

pub_type

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