TRIIODOTHYRONINE ATTENUATES ESTRADIOL-INDUCED INCREASES IN DOPAMINE D-2 RECEPTOR NUMBER IN RAT ANTERIOR-PITUITARY

Estrogens promote adenohypophyseal enlargement and tumor transformatio n, and thyroid hormones antagonize these effects. Hormone-induced pitu itary enlargement may be mediated by alterations in pituitary dopamine rgic function. The present study examined the effects of chronic (20 d ays) administration of estradiol benzoate (EB), triiodothyronine (T3), or EB and T3 (T3 + EB) on dopamine (D-2) receptors in rat anterior pi tuitary. D-2 receptor number increased after EB without altered recept or affinity. T3 alone did not affect D-2 receptor number in the anteri or pituitary but significantly attenuated the effect of EB. T3 adminis tration also inhibited EB-induced anterior pituitary hyperplasia. D-2 receptor upregulation by EB more likely could reflect a compensatory r esponse to decreased receptor occupation. The present results suggest that D-2 receptors could play an important role in estrogen-induced ad enohypophyseal tumor formation and hyperprolactinemia and that thyroid hormones may inhibit estrogen-induced pituitary tumor development via adenohypophyseal D-2 receptors.