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In order to investigate the relationship between the increment of plasma prolactin (PRL) levels and the change of plasma levels of PRL, DHEA-S, cortisol, aldosterone and 17 alpha OH delta 5-P were quantified by respective RIA in patients treated with TRH parenterally or with sulpiride orally. The results were as follows: During the infusion of TRH, plasma levels of PRL reached the maximal values within 30 min and then declined gradually in spite of continued TRH stimulation. Sulpiride given orally for 12 consecutive days in the luteal phase of the menstrual cycle caused a significant increase in the plasma PRL level. This increase was higher than that obtained in the experiment during the follicular phase. No significant change in the plasma level of 17 alpha OH delta 5-P was observed TRH sulpiride administration. In 3 out of 9 cases, plasma DHEA-S levels were elevated significantly on day 13 to 14 of the experimental course. These results indicate that the responsiveness of plasma levels of adrenal androgens to the raised plasma PRL level requires a certain period of time in the hyperprolactinemic state in the human female.

Sixteen normal pregnant woman at delivery were administered 10 mg of Metoclopramide (MCP) intravenously, and the Prolactin (PRL) levels in the maternal plasma and in the amniotic fluid were measured by RIA before and after the administration, and in the umbilical plasma after the administration. Eight other pregnant women at term were studied similarly without the administration of MCP and served as the control. In this experiment, there was a significant increase only in the maternal plasma PRL but not in the amniotic fluid PRL nor in the umbilical plasma PRL. Furthermore, by using an intrauterine pressure catheter and a maternal intravenous cannula we measured the amniotic fluid PRL and the maternal plasma PRL about every 20 minutes during 3 hours before and after the intravenous administration of MCP 10mg. The maternal plasma PRL increased promptly and remained high for 150 minutes, while there was no significant change in the amniotic fluid PRL. This obvious discrepancy supports the hypothesis that decidua is the source of amniotic fluid PRL and suggests an independent regulation of amniotic fluid PRL.

Alterations of plasma TSH and PRL levels following various types of administration with TRH were studied in the luteal phase of women with normal menstrual cycles. The results were as follows: Plasma PRL response to a single i.v. injection of tRH with DHEA-S drop injection was not significantly different from that observed without it. The data suggest that DHEA-S does not affect the feedback mechanism in the short-term course of the experiment. Alterations in the plasma levels of PRL during intermittent as well as continuous infusion with TRH were quite different from those with TSH. Plasma TSH increased following the beginning of a continuous infusion with TRH and reached a peak at approximately 180 min, maintaining a plateau until the infusion was withheld. On the other hand, plasma PRL levels increased rapidly to reach peak levels in 30 min after the start of the infusion gradually following a decline in spite of continued TRH stimulation. Furthermore, a stepwise increase of TSH levels was observed following 4 intermittent injections of TRH; however, plasma PRL rapidly reached peak levels in 30 min following the 1st injection of TRH and a further 3 injections did not raise the levels of PRL. The results suggest that in humans, the synthesis and release of PRL occur independently in the pituitary.