Effects of testosterone, dihydrotestosterone, and estradiol on the impaired prolactin response to metoclopramide in the castrated rat.

Effects of testosterone, dihydrotestosterone, and estradiol on the impaired prolactin response to metoclopramide in the castrated rat.
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睾酮、二氢睾酮和雌二醇对去势大鼠催乳素对胃复安反应受损的影响。

DOI:
10.1095/biolreprod25.1.6
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发表时间:
1981
影响因子:
3.6
通讯作者:
I. Spitz
I. Spitz
中科院分区:
生物学2区
文献类型:
--
作者:
E. Zylber;H. Gershman;I. Spitz

文献摘要

被引文献

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本研究旨在评估三种睾丸类固醇激素,睾酮,双氢睾酮和雌二醇对去势大鼠PRL分泌的影响。这是通过评价雄激素和雌激素及其拮抗剂,单独或组合,对甲氧氯普胺(MET)诱导的去势雄性大鼠PRL分泌的影响。用丙酸睾酮(TP)和双氢睾酮(DHT)处理去势大鼠后,前列腺和精囊腺保持正常重量。抗雄激素醋酸环丙孕酮(CA)本身无作用,可部分拮抗这种作用。TP,以及DHT和EB,防止血浆和垂体LH和血浆FSH的升高,随后去势。CA部分钝化TP和完全阻断DHT的效果,表明它作为一种抗雄激素。盐酸萘福昔定(NH)可拮抗EB对促性腺激素的作用,但不拮抗TP对促性腺激素的作用。这表明,在与EB,NH作为抗雌激素的组合。去势大鼠对MET的PRL反应明显降低(P<0.001)。TP,DHT和CA的管理部分恢复PRL分泌正常。当去势大鼠接受TP与CA组合时,实现了正常反应。然而,DHT/CA组合仅部分恢复PRL反应。NH单独给药也部分恢复PRL分泌正常。当去势大鼠接受TP与NH的组合,他们的反应是无法区分的控制。EB产生了显着夸大的反应,但当与NH结合使用时,抗雌激素抑制EB对PRL对MET反应的影响。它的结论是,TP,如DHT,同时保持附属性器官的重量,只有部分恢复PRL反应。CA对PRL分泌也有类似的影响,但不影响附属性器官重量。当NH单独给药时,它是一种弱雌激素激动剂。与EB联合使用时,它可作为抗雌激素并减弱EB对PRL对MET反应的影响。相反,当给予TP时,对PRL反应有协同作用。这表明,睾酮和双氢睾酮不是唯一负责维持雄性大鼠的PRL分泌,推测还需要其他睾丸产物。
This study was designed to assess the effect of three testicular steroids, testosterone, dihydrotestosterone, and estradiol, on PRL secretion in castrated rats. This has been done by evaluating the effect of androgens and estrogens and their antagonists, alone or in combination, on metoclopramide (MET)-induced PRL secretion in the castrated male rat. Ventral prostate and seminal vesicles retained normal weight after treatment of castrated rats with testosterone propionate (TP) and dihydrotestosterone (DHT). This effect was partially antagonized by the antiandrogen cyproterone acetate (CA) which in itself had no effect. TP, as well as DHT and EB, prevented the rise of plasma and pituitary LH and plasma FSH consequent to castration. CA partially blunted the TP and completely blocked the DHT effect, indicating that it acts as an antiandrogen. Nafoxidine hydrochloride (NH) antagonized the effect of EB, but not of TP on gonadotropins. This indicates that in combination with EB, NH acts as an antiestrogen. The PRL response to MET was significantly reduced in castrated rats (P<0.001, compared with controls). Administration of TP, DHT, and CA partially restored PRL secretion to normal. When castrated rats received TP in combination with CA, a normal response was achieved. However, the DHT/CA combination only partially restored the PRL response. Administration of NH alone also partially restored PRL secretion to normal. When castrated rats received TP in combination with NH, their response was indistinguishable from controls. EB produced a markedly exaggerated response, but when given in combination with NH, the antiestrogen inhibited the effect of EB on the PRL response to MET. It is concluded that TP, like DHT, while maintaining the weight of the accessory sex organs, only partially restored the PRL response. A similar effect on PRL secretion was observed with CA, which did not affect accessory sex organ weight. When NH was administered alone, it was a weak estrogen agonist. In combination with EB, it acted as an antiestrogen and attenuated the effect of EB on the PRL response to MET. In contrast, when given with TP, there was a synergistic effect on the PRL response. This suggests that testosterone and dihydrotestosterone are not solely responsible for the maintenance of PRL secretion in the male rat and that other testicular products are presumably also required.