Nedvídková J, Pacák K, Nedvídek J, Goldstein D S, Schreiber V
Institute of Endocrinology, Prague, Czech Republic.
Brain Res. 1996 Mar 11;712(1):148-52. doi: 10.1016/0006-8993(95)01524-8.
Estrogens promote adenohypophyseal enlargement and tumor transformation, and thyroid hormones antagonize these effects. Hormone-induced pituitary enlargement may be mediated by alterations in pituitary dopaminergic function. The present study examined the effects of chronic (20 days) administration of estradiol benzoate (EB), triiodothyronine (T3), or EB and T3 (T3 + EB) on dopamine (D-2) receptors in rat anterior pituitary. D-2 receptor number increased after EB without altered receptor affinity. T3 alone did not affect D-2 receptor number in the anterior pituitary but significantly attenuated the effect of EB. T3 administration also inhibited EB-induced anterior pituitary hyperplasia. D-2 receptor upregulation by EB more likely could reflect a compensatory response to decreased receptor occupation. The present results suggest that D-2 receptors could play an important role in estrogen-induced adenohypophyseal tumor formation and hyperprolactinemia and that thyroid hormones may inhibit estrogen-induced pituitary tumor development via adenohypophyseal D-2 receptors.
雌激素可促进腺垂体增大和肿瘤转化，而甲状腺激素则拮抗这些作用。激素诱导的垂体增大可能由垂体多巴胺能功能的改变介导。本研究检测了长期（20天）给予苯甲酸雌二醇（EB）、三碘甲状腺原氨酸（T3）或EB与T3联合用药（T3 + EB）对大鼠垂体前叶多巴胺（D-2）受体的影响。给予EB后D-2受体数量增加，而受体亲和力未改变。单独给予T3对垂体前叶D-2受体数量无影响，但可显著减弱EB的作用。给予T3还可抑制EB诱导的垂体前叶增生。EB导致的D-2受体上调更可能反映了对受体占据减少的一种代偿反应。目前的结果表明，D-2受体可能在雌激素诱导的腺垂体肿瘤形成和高催乳素血症中起重要作用，且甲状腺激素可能通过腺垂体D-2受体抑制雌激素诱导的垂体肿瘤发展。
