Dose-dependent suppression of postcastration luteinizing hormone secretion exerted by exogenous prolactin administration in male rats: a model for studying hyperprolactinemic hypogonadism.
Dose-dependent suppression of postcastration luteinizing hormone secretion exerted by exogenous prolactin administration in male rats: a model for studying hyperprolactinemic hypogonadism.
复制标题
雄性大鼠外源性催乳素给药对去势后黄体生成激素分泌的剂量依赖性抑制：研究高催乳素性性腺功能减退症的模型。
DOI：
10.1159/000125748
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发表时间：
1991
影响因子：
4.1
通讯作者：
Selmanoff,M
中科院分区：
文献类型：
--
作者：
Park,SK;Selmanoff,M
我们研究了急性高催乳素血症对成年雄性大鼠去势后平均黄体生成素(LH)水平升高的抑制作用。从去势时开始，每隔12小时在聚乙烯吡咯烷酮储存库中皮下注射纯化的绵羊催乳素(OPRL)，持续96小时。OPRL在24-72小时内抑制去势后的黄体生成素分泌，当oPRL水平升高时，这种作用自发逆转。OPRL以分级、剂量依赖的方式抑制去势后黄体生成素的分泌。给大鼠递增剂量的oPRL，并在48小时后进行研究，这是黄体生成素抑制最大的时间。第一种显著的抑制作用始于高生理范围(约200 ng/ml)，并持续到循环中oPRL水平的病理生理肿瘤范围(约2500 ng/ml)。高水平的oPRL显著抑制去势后黄体生成素的释放。在剂量效应研究中，研究了oPRL对大鼠内源性PRL分泌的自我调节反馈作用。令人惊讶的是，发现PRL自动反馈似乎是作为一个阈值来调节的，而不是分级的剂量反应，更重要的是，产生第一次显著抑制黄体生成素分泌的oPRL剂量与施加PRL自动反馈的剂量相同。这些发现表明，去势后黄体生成素的分泌受到循环PRL滴度(约200 ng/ml)的抑制，该滴度高于基础水平和应激诱导水平，但在怀孕、假孕和哺乳期遇到的范围内。此外，一个常见的下丘脑机制(可能是多巴胺能)，在这个范围内被升高的oPRL水平激活，可能会抑制黄体生成素和大鼠催乳素的分泌。
We examined the inhibitory effects of acute hyperprolactinemia on the postcastration rise in mean luteinizing hormone (LH) levels in adult male rats. The animals were administered purified ovine prolactin (oPRL) subcutaneously in a polyvinyl-pyrrolidone depot every 12 h for 96 h, beginning at the time of castration. oPRL suppressed postcastration LH secretion from 24 to 72 h when the effect spontaneously reversed in the face of elevated oPRL levels. oPRL suppressed postcastration LH secretion in a graded, dose-dependent fashion. The rats were administered increasing doses of oPRL and studied 48 h later, a time of maximal LH suppression. The first significant inhibition began in the high physiological range (about 200 ng/ml) and continued into the pathophysiological tumor range (about 2,500 ng/ml) of circulating oPRL levels. The highest oPRL levels markedly suppressed postcastration LH release. Autoregulatory feedback of oPRL on endogenous rat PRL secretion was examined in the dose-response study. It was striking to discover that PRL autofeedback appeared regulated as a threshold instead of a graded dose response and, more importantly, that the oPRL dose which produced the first significant suppression of LH secretion was the same dose which exerted PRL autofeedback. These findings indicate that postcastration LH secretion is inhibited by circulating PRL titers (about 200 ng/ml) which are above basal and stress-induced levels, but are within the range encountered during pregnancy, pseudopregnancy, and lactation. In addition, a common hypothalamic mechanism (perhaps dopaminergic), activated by elevated oPRL levels in this range, may inhibit both LH and rat PRL secretion.