The effect of estrogen on the dopaminergic control of PRL secretion was investigated. Treatment of ovariectomized rats with estradiol benzoate (25 μg/kg, sc) daily for 5 days resulted in a marked elevation of the serum PRL concentration. This estrogen-induced increase in serum PRL levels was apparently not the result of a suppressed release of dopamine into hypophysial portal blood, since the mean dopamine concentration in hypophysial portal plasma in estrogen-treated rats was 2.5 times that in vehicle-treated animals. It was found that under in vitro conditions, dopamine was much less effective in inhibiting the release of PRL from pituitary glands of estrogen-treated rats than from glands of vehicle-treated controls. The capacity of PRL cells to internalize dopamine and incorporate it into PRL secretory granules was evaluated in anterior pituitary tissue obtained from estrogen- or vehicle-treated animals. When tissue fragments of the anterior pituitary gland were incubated in the presence of dopamine (105 M) for 30 min at 37 C and then homogenized and fractionated by means of continuous sucrose density gradient centrifugation, it was found that the amount of dopamine associated with PRL granules from anterior lobe tissue of estrogen-treated rats was only 40% of that from the tissue of vehicle-treated controls. These results are supportive of the hypothesis that the ability of estrogen to antagonize the inhibitory action of dopamine on PRL secretion is mediated through an estrogen-induced reduction in the capacity of the PRL cell to incorporate dopamine into PRL secretory granules. (Endocrinology 108: 440, 1981).
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