Acute progesterone and 17 beta-estradiol modulation of luteinizing hormone secretion by pituitaries of cycling rats superfused in vitro.
Acute progesterone and 17 beta-estradiol modulation of luteinizing hormone secretion by pituitaries of cycling rats superfused in vitro.
复制标题
体外灌注循环大鼠垂体黄体生成素分泌的急性黄体酮和 17β-雌二醇调节。
作者：
J. Turgeon;D. W. Waring
在大鼠动情周期期间，血清17β-雌二醇(E2)和黄体酮的浓度发生显着变化。本研究的目的是检查 E2 和黄体酮对 4 天周期每个阶段 1230 小时时获得的离体垂体的急性影响。在零时间，将单四分之一的垂体前叶放入室中，并以0.5ml/min的速度用含有或不含有类固醇的培养基199灌注360分钟；连续 10 分钟收集流出物样品。在 120 分钟和 240 分钟时以两次连续 10 分钟脉冲的方式给予 LHRH (10 ng/ml)。体外发情前期和动情间期 II 期垂体表现出特征性的 LHRH 自启动反应：在灌注介质中存在和不存在类固醇的情况下，对第二次 LHRH 脉冲的 LH 分泌反应增加；然而，当 E2 (50 pg/ml) 存在时，对 LHRH 初始脉冲的反应幅度显着降低。黄体酮 (50 ng/ml) 的存在导致 LHRH 第一次脉冲的 LH 分泌反应显着增强；当灌注培养基中同时含有E2和孕酮时，孕酮的刺激作用减弱。体外类固醇暴露 60 分钟后，黄体酮会增强 LHRH 诱导的 LH 分泌，但仅暴露 10 分钟后就无法证明。在没有类固醇的情况下，放线菌酮抑制黄体酮增加和 LHRH 自启动，而不影响 LH 对初始 LHRH 脉冲的分泌反应。发情期和动情间期-I 未观察到黄体酮增加。然而，培养基中 E2 的存在导致发情期或动情间期-I 垂体对 LHRH 第一次脉冲的反应显着降低。这些数据 1) 证明 E2 本身抑制发情前期垂体 LHRH 诱导的 LH 分泌，2) 提供了在缺乏 E2 的情况下孕酮对发情前期垂体的直接刺激作用的证据，并表明孕酮在排卵前 LH 激增期间具有正反馈作用。 （内分泌学 108：413，1981）
During the rat estrous cycle there are marked changes in the concentrations of serum 17 beta-estradiol (E2) and progesterone. The objective of the present study was to examine the acute effects of E2 and progesterone on isolated pituitaries obtained at 1230 h at each stage of the 4-day cycle. At time zero, single quartered anterior pituitaries were placed in a chamber and superfused at 0.5 ml/min with medium 199 with or without steroids for 360 min; sequential 10-min effluent samples were collected. LHRH (10 ng/ml) was administered as two successive 10-min pulses at 120 and 240 min. The proestrous and the diestrous-II pituitaries in vitro exhibited the characteristic LHRH self-priming response: an increased LH secretory response to a second pulse of LHRH in both the absence and presence of steroids in the superfusion medium; however, the magnitude of the response to the initial pulse of LHRH was reduced significantly when E2 (50 pg/ml) was present. The presence of progesterone (50 ng/ml) resulted in a marked augmentation of the LH secretory response to the first pulse of LHRH; when both E2 and progesterone were included in the superfusion medium, the stimulatory effect of progesterone was reduced. The progesterone augmentation of LHRH-induced LH secretion was present after 60 min of steroid exposure in vitro but was not demonstrable after only 10 min of exposure. Cycloheximide inhibited the progesterone augmentation and the LHRH self-priming without affecting the LH secretory response to the initial LHRH pulse in the absence of steroid. Progesterone augmentation was not observed on estrus and diestrous-I. The presence of E2 in the medium, however, resulted in a significant decrease in the response to the first pulse of LHRH for pituitaries from either estrus or diestrous-I. These data 1) demonstrate that E2 by itself suppresses LHRH-induced LH secretion by the proestrous pituitary and 2) provide proof for a direct stimulatory action of progesterone, in the absence of E2, on the proestrous pituitary and suggest a positive feedback role for progesterone during the preovulatory LH surge. (Endocrinology 108: 413, 1981)