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Increased Dopaminergic Activity Inhibits Basal and Metoclopramide- Stimulated Prolactin and Thyrotropin Secretion^*

Department of Internal Medicine and Endocrinology, Herlev Hospital, University of Copenhagen 2730 Herleu Department of Obstetrics and Gynecology, Rigshospitalet, University of Copenhagen 2100 Copenhagen; Hvidovre Hospital, University of Copenhagen 2650 Hvidovre, Denmark

Address all correspondence and requests for reprints to: Dr. Claus Hagen, Department of Internal Medicine and Endocrinology, Herlev Hospital, 2730 Herlev, Denmark.

The influence of physiological to pharmacological doses of dopamine (DA) on basal and metoclopramide(MTC)-stimulated PRL and TSH secretion was studied in 11 regularly menstruating women between days 3 and 8 of the cycle. In groups of 6, the women received 5-h infusions of either 5% glucose or DA in a solution of 5% glucose at a rate of 12–16ml/h, adjusted according to weight. Infusion rates of DA were 0.04 µg/kg·min (low), 0.4 µg/kg·min (medium), and 4.0 µg/kg·min (high). After 3 h of infusion, 10 mg MTC were given iv. Blood samples were collected every 15 min from 1 h before to 2 h after the infusion, for a total of 8 h, for measurements of PRL and TSH.

The mean serum PRL concentrations declined significantly (P < 0.05) during DA infusions to nadir values of 62 ± 5% (± SEM; low), 43 ± 3% (medium), and 43 ± 6% (high) of the basal levels, whereas basal TSH levels declined significantly, to 64 ± 5% of basal levels (P < 0.05), during both the medium and high dose DA infusions. On paired comparisons, the hormone responses to MTC were lower (P < 0.05) during the infusion of high dose DA (PRL, 2286 ± 495% vs. 891 ± 328%; TSH, 100 ± 43% vs. 60 ± 15%), but were not changed when MTC was given during the low and medium doses of DA. A rebound phenomenon was found for PRL (P < 0.05) after the medium and high doses of DA and for TSH (P < 0.05) after the high dose.

These results indicate that doses of DA considered physiological inhibit PRL and TSH secretion and larger doses inhibit their responses to the DA antagonist MTC.

^* This work was supported by grants from the Danish Medical Research Council, Gerda and Aage Haensch's Foundation, and P. Carl Petersens Foundation.

Received September 16, 1985.

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