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Biology of Reproduction, Vol 23, 264-270, Copyright © 1980 by Society for the Study of Reproduction
1 Oregon Regional Primate Research Center,
Beaverton, Oregon 97006
and
Department of Physiology, University of Oregon Health Sciences Center,
Portland, Oregon 97201 To test the hypothesis that a fetoplacental unit for estrogen biosynthesis is operative in the
rhesus monkey, studies were performed in chronically catheterized animals during late gestation.
Changes in fetal and maternal plasma concentrations of estrone, estradiol, dehydroepiandrosterone
sulfate (DHEAS), and androstenedione were determined in response to infusions of dexamethasone
into mothers, and of ACTH, DHEAS, or androstenedione into fetuses. A significant (P<0.0l) maternal: fetal concentration difference ( Administration of DHEAS or androstenedione to fetuses without concurrent dexamethasone
administration increased (P<0.05) fetal estrone and maternal estrone and estradiol. No significant
changes (P>0.05) were observed in maternal or fetal cortisol or progesterone concentrations. Fetal
estradiol levels were relatively low in all of the experiments, and they were not significantly altered
by dexamethasone, ACTH, DHEAS, or androstenedione infusions (P>0.05). Collectively, these data indicate that the increases in fetal and maternal estrogens after administration of ACTH to fetuses are the result of ACTH stimulation of fetal adrenal DHEAS and
androstenedione production. Androstenedione and DHEAS are transported via the fetal circulation
to the placenta, where they are converted to estrogens. Thus, the rhesus monkey, like the human,
has a functional fetoplacental unit.
2 Department of Pediatrics,
University of California at San Francisco,
San Francisco, California 94143
3 Oregon Regional Primate Research Center,
Beaverton, Oregon 97006
and
Department of Obstetrics and Gynecology,
University of Oregon Health Sciences Center,
Portland, Oregon 97201
20:1) was observed in control
samples for estradiol, but not for estrone, DHEAS, or androstenedione (P>0.05). Dexamethasone
administration decreased (P<0.05) maternal estrone, estradiol, and DHEAS, as well as fetal estrone
and DHEAS. Subsequent administration of ACTH to fetuses increased (P<0.05) fetal estrone,
DHEAS and androstenedione, and also maternal estrone and estradiol. Fetal estradiol and maternal
DHEAS and androstenedione were not significantly changed (P>0.05). The concentrations of fetal
estrone and DHEAS, and of maternal estrone and estradiol returned to pre-dexamethasone control
values during infusion of ACTH into fetuses.
Note:
ACKNOWLEDGMENTS
We gratefully acknowledge the expert technical
assistance of Michael Cook, Sandra Buzzetti, and
Carole Thomas.
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