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The human adrenal cortex secretes a variety of androgens, as shown in Fig. 1, in addition to cortisol and aldosterone. Some of these steroids function as androgens, or serve as precursors for androgen or estrogen formation in peripheral tissues. The control of glucocorticoid and mineralocorticoid secretion is largely under the influence of ACTH and the renin-angiotensin system, respectively. However, the mechanism of control of adrenal androgen (AA) secretion is less well defined, and is the main subject of this review. ACTH is the most widely accepted modulator of AA secretion at present. Rosenfield et al. (1) studied endogenous cortisol and dehydroepiandrosterone (DHA) secretion in a normal volunteer and found a correlation between the rhythmicity of secretion of cortisol and DHA, although the magnitude of the DHA rhythm was much less than that of cortisol. Other investigators have administered bovine ACTH or synthetic forms such as the peptide-(l–24) cosyntropin directly, in order to assess their ability to cause acute secretion of AA. These studies are summarized in Table 1. Irvine et al. (2) reported an increase in plasma androstenedione (A) after intramuscular cosyntropin given to healthy male volunteers. A similar response of A to cosyntropin was found by Cowley et al. (3) in a man with prostatic carcinoma after orchiectomy. These results confirm earlier studies by Chapdelaine et al. (4) using measurements of A by double isotope derivative techniques.
Parker et al. (Wed,) studied this question.