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Acetylcholine-induced catecholamine secretion from isolated, perfused bovine adrenal medulla was strongly inhibited by hydrocortisone (30 micro M), estradiol (30 micro M), and estriol (30 micro M). Diethylistilbestrol (DES) (10 and 30 micro M) inhibited acetylcholine-induced secretion, and the effect of the higher dose was prolonged. Inhibition of high potassium-induced secretion by DES (30 micro M) indicated that hormonal inhibition of evoked secretion was not by competition for acetylcholine-sensitive receptor sites. Dehydrotestosterone (30 micro M) was ineffective in inhibiting acetylcholine-induced secrection. Hydrocortisone, estradiol, and estriol treatments enhanced nonstimulated release. It is suggested that incorporation of certain steroid into plasma and granule membranes, thereby modifying membrane function, enhances nonstimulated release and may also block evoked release of secretoy material.
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Wiechman et al. (2008) studied this question.
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