INHIBITION OF ESTROGEN-INDUCED ANTERIOR-PITUITARY ENLARGEMENT AND ARTERIOGENESIS BY BROMOCRIPTINE IN FISCHER-344 RATS

INHIBITION OF ESTROGEN-INDUCED ANTERIOR-PITUITARY ENLARGEMENT AND ARTERIOGENESIS BY BROMOCRIPTINE IN FISCHER-344 RATS
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DOI:
10.1210/endo-120-2-617
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发表时间:
1987-02-01
期刊:
影响因子:
4.8
通讯作者:
WEINER, RI
WEINER, RI
中科院分区:
医学2区
文献类型:
--
作者:
ELIAS, KA;WEINER, RI

文献摘要

被引文献

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在Fischer 344大鼠中研究了多巴胺(DA)调节和垂体前叶(AP)血供变化在雌二醇(E2)诱导的垂体细胞增殖病因学中的相互关系。大鼠植入E2填充或空的硅橡胶胶囊21天,单独或与强效DA激动剂溴隐亭(CB-154)的颗粒结合。测定AP血管化、正中隆起DA含量和培养AP细胞对DA反应性的变化。通过注射仅能通过新形成的动脉(动脉生成)到达AP的15 μ m微球来评估直接动脉血液供应的发展。将AP酶促分散并培养3天,然后用增加浓度的DA攻击3小时。放射酶法测定DA含量,放射免疫法测定血清PRL。E2治疗增加垂体的重量,血清PRL水平,和微球的数量在AP 4.5-,173-和142倍,分别超过对照值。中位隆起DA含量下降71%,E2治疗,而DA抑制PRL分泌的能力在体外从最大的70%下降到40%,ED 50没有变化。同时用CB-154处理显著降低E2对动脉生成、垂体重量、血清PRL水平和正中隆起DA含量的影响。阻断增加多巴胺能刺激E2诱导的AP扩大与动脉生成的抑制密切相关,这进一步表明血管变化在催乳素细胞增殖中的重要作用。
The interrelationship between dopamine (DA) regulation and changes in the blood supply of the anterior pituitary lobe (AP) in the etiology of estradiol (E2)-induced proliferation of pituitary cells was studied in Fischer 344 rats. Rats were implanted with E2-filled or empty Silastic capsules for 21 days alone or in conjunction with pellets of the potent DA agonist bromocriptine (CB-154). Changes in vascularization of the AP, median eminence DA content, and responsiveness to DA of cultured AP cells were measured. Development of a direct arterial blood supply was assessed by the injection of 15-.mu.m microspheres that can only reach the AP by newly formed arteries (arteriogenesis). APs were enzymatically dispersed and cultured for 3 days before challenges with increasing concentrations of DA for 3 h. DA content was measured by radioenzymatic assay, and serum PRL was determined by RIA. E2 treatment increased the weight of the pituitary gland, serum PRL levels, and the number of microspheres in the AP 4.5-, 173-, and 142-fold, respectively, over control values. Median eminence DA content was decreased 71% by E2 treatment, while the ability of DA to suppress PRL secretion in vitro decreased from a maximum of 70% to 40% with no change in the ED50. Simultaneous treatment with CB-154 dramatically decreased the effect of E2 on arteriogenesis, pituitary weight, serum PRL levels and median eminence DA content. Blockade of E2-induced AP enlargement by increased dopaminergic stimulation was closely correlated with inhibition of arteriogenesis, which further suggests an important role for vascular changes in lactotroph proliferation.