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The Effect of 17ß-Estradiol on Adrenocortical Sensitivity, Responsiveness, and Steroidogenesis in Postmenopausal Women¹

Department of Obstetrics and Gynecology, Division of Reproductive Biology and Endocrinology, University of Alabama at Birmingham, Birmingham, Alabama 35233

Address all correspondence and requests for reprints to: C. R. Parker, Jr., Ph.D., Department of Obstetrics and Gynecology, Division of Reproductive Biology and Endocrinology, 618 20th Street South, University of Alabama at Birmingham, Birmingham, Alabama 35233-7333.

Aging in women is associated with reduced production of adrenal androgens (AAs); this decrease may in part be the result of menopausal hypoestrogenism. To determine the effects of physiological concentrations of estradiol (E₂) on adrenocortical sensitivity and responsiveness in postmenopausal women, we determined steroid responses to a continuous incremental ACTH-(1–24) infusion (0, 20, 40, 80, 160, 320, 640, and 1280 ng/1.5 m²/h), followed by an ACTH-(1–24) bolus of 0.25 mg, after overnight dexamethasone suppression before and after 3 months of E₂ therapy (transdermal E₂, 0.05 mg/day) in 14 postmenopausal women. After E₂ treatment, subjects demonstrated an increase in serum E₂ concentrations from 29.8 ± 2.6 to 49.9 ± 6.0 pg/mL (P < 0.005) and a decline in mean FSH levels from 83.1 ± 24.4 to 57.5 ± 17.3 mIU/mL (P < 0.004). E₂ administration had no effect on basal, postdexamethasone, or maximally stimulated serum levels of cortisol (F), dehydroepiandrosterone (DHEA), androstenedione (A⁴), or 17-hydroxyprogesterone (17-OHP). Furthermore, E₂ did not affect adrenal sensitivity or responsiveness to ACTH-(1–24) stimulation. Finally, the steroid ratios reflecting 3ß-hydroxysteroid dehydrogenase (i.e. the A⁴/DHEA ratio) and ⁴17,20-lyase (i.e. the A⁴/17-OHP ratio) activities also were unaffected by E₂ therapy. The responsiveness of F to ACTH was significantly greater than that of DHEA, A⁴, or 17-OHP regardless of the circulating E₂ levels. Furthermore, F and A⁴ were significantly more sensitive to ACTH stimulation than were 17-OHP and DHEA, and this was not altered by E₂ administration. We conclude that transdermal E₂ replacement to postmenopausal women does not significantly alter AA sensitivity or responsiveness to ACTH. Hence, it is unlikely that the hypoestrogenism of menopause contributes to the decline in AAs noted with age. Furthermore, menopausal estrogen replacement, at least in physiological amounts administered transdermally, cannot be expected to reverse the suppressed production of these androgens.

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