Endocrinology, Vol 108, 489-494, Copyright © 1981 by Endocrine Society

ARTICLES

Dopamine in hypophysial stalk blood of the rhesus monkey and its role in regulating prolactin secretion

JD Neill, LS Frawley, PM Plotsky and GT Tindall

Numerous studies are suggestive of dopamine serving as the hypothalamic PRL-inhibiting factor in the monkey. In the present study, we measured dopamine concentrations in plasma collected from the hypophysial stalk and determined whether those concentrations were sufficient to account for the inhibiting effect on PRL secretion exerted by the hypothalamus. First, we collected hypophysial stalk blood from seven follicular phase monkeys (four anesthetized with pentobarbital and three with phencyclidine) using a transorbital surgical approach. Dopamine concentrations, measured with a liquid chromatographic-electrochemical procedure, averaged 0.76 ng/ml in stalk plasma and less than 0.1 ng/ml in peripheral plasma collected contemporaneously. Next, we determined the rate of dopamine infusion required to produce peripheral plasma concentrations of dopamine similar to those measured in hypophysial stalk plasma. In seven monkeys, a dopamine infusion rate of 0.1 microgram/kg BW . min produced plasma dopamine concentrations of 0.62 ng/ml, whereas a 10-fold higher rate (1.0 microgram/kg . min) produced plasma concentrations of 1.95 ng/ml. Then, we infused these doses of dopamine into intact follicular phase animals, stalk-transected animals, and estrogen-treated stalk-transected animals to determine their effect on PRL release. The physiological dose of dopamine (0.1 microgram/kg . min) significantly suppressed plasma PRL levels in intact follicular phase animals and estrogen-treated stalk-transected animals but not in untreated stalk-transected animals. The higher rate of dopamine infusion (1.0 microgram/kg . min) was required to inhibit PRL release in the latter group. These results demonstrate that dopamine is secreted by the hypothalamus into hypophysial portal blood in quantities sufficient to account for much of the PRL-inhibiting activity known to be caused by the hypothalamus. Moreover, the results suggest that estrogen reinforces the inhibitory effect of dopamine on PRL release in primates, in contrast to its antagonistic effect in rodents. (Endocrinology 108: 489, 1981)

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