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Journal of Clinical Endocrinology & Metabolism Vol. 51, No. 5 1019-1025
doi:10.1210/jcem-51-5-1019
Copyright © 1980 by the Endocrine Society.
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Dopamine and Prolactin in Human Pregnancy*

NIRA BEN- JONATHAN{dagger} and ROBERT A. MUNSICK

Departments of Physiology and Obstetrics and Gynecology, Indiana University School of Medicine, Indianapolis, Indiana 46223

Address all correspondence and requests for reprints to: Dr. Nira Ben-Jonathan, Department of Physiology, Indiana University School of Medicine, 1100 West Michigan Street, Indianapolis, Indiana 46223.

The interrelationship between dopamine and PRL during human pregnancy was investigated. Amniotic fluid collected from 104 pregnant women of different gestational ages was analyzed for dopamine by a radioenzymatic assay and for PRL by a RIA. The PRL concentration during the first trimester was 380 ng/ml, rose to approximately 5000 ng/ml during the second and third trimesters, and decreased to 1090 ng/ml near term. Dopamine in the amniotic fluid was approximately 1.1 ng/ ml throughout most of gestation, but rose to 2.4 ng/ml near term. Norepinephrine was low or undetectable (<0.12 ng/ml) during most of gestation, but increased to 0.4 ng/ml at term. Epinephrine was undetectable in all samples. The amniotic fluid also contained significant amounts of conjugated dopamine and norepinephrine, the levels of which rose near term. Dopamine in cord plasma from fetuses was 2.0 ng/ml, which was twice that in plasma from parturients or nonpregnant women. Norepinephrine levels (0.6-0.9 ng/ml) were similar in the fetal and maternal circulations.

To determine if amniotic fluid dopamine was biologically active, dispersed rat pituitary cells were used. Dopamine (10-8 and 10-7 M) caused a 35% and 80% inhibition of PRL secretion, respectively. Acidic extracts of human amniotic fluid caused 60-80% suppression of PRL secretion in a dose-dependent manner. Since the decidua is one of the possible sources of amniotic fluid PRL, human decidual explants were subjected to short term incubation. Decidua from midgestation released twice the amount of PRL as decidua at term. However, dopamine at the range of concentrations found in human amniotic fluid was incapable of reducing decidual PRL secretion in vitro.

The following conclusions were drawn. 1) There is a reciprocal relationship between dopamine and PRL in human amniotic fluid; at term, the concentration of dopamine rises markedly, whereas that of PRL falls. The high levels of dopamine in fetal plasma and the presence of its conjugated compound in the amniotic fluid suggest that amniotic fluid dopamine originates from the fetal compartment, possibly via the fetal urine. 2) Dopamine in human amniotic fluid is biologically active, as judged by its ability to inhibit rat pituitary PRL secretion. However, dopamine itself is incapable of inhibiting human decidual PRL secretion in vitro, suggesting that the decidua might not be one of its target tissues.

* This work was supported by NIH Grants NS-13234 and AM-20542, Diabetes Research and Training Center, and a grant from the American Diabetes Association. It was presented in part at the 61st Annual Meeting of The Endocrine Society, Anaheim, CA, June 1979.

{dagger} Recipient of Research Career Development Award NS-219.

Received December 7, 1979.




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