Lafuente A, Marcó J, Esquifino A I
Department of Toxicology, Faculty of Sciences, University of Vigo, Orense, Spain.
Proc Soc Exp Biol Med. 1995 Jun;209(2):163-9. doi: 10.3181/00379727-209-43891.
It is well known that LH is released in an episodic fashion. However, the effects of hyperprolactinemia on luteinizing hormone (LH) pulsatility are not fully understood. The present study was undertaken to describe hyperprolactinemia effects on the regulatory mechanism of LH pulsatility. For this purpose hyperprolactinemia was induced in female rats by the transplantation of two pituitary glands beneath the kidney capsule. Age-matched sham-operated animals were used as controls. We have evaluated the pulsatile pattern of LH in both groups of animals. As expected, pituitary grafting increased mean serum prolactin levels compared with the values found in control animals. Luteinizing hormone-releasing hormone (LHRH) administration did not change serum prolactin levels in control or in pituitary-grafted rats. Thyrotropin-releasing hormone (TRH) administration increased prolactin secretion in both groups. There is an increase in mean values of LH and in the absolute amplitude of LH peaks in pituitary-grafted compared with control rats. No other parameters of LH pulsatility were changed by pituitary grafting. After LHRH administration, LH release was increased and a priming effect after the second administration of LHRH is observed in control rats. In pituitary-grafted animals the responses of LH to LHRH administration was diminished compared with the response observed in control rats. The administration of two pulses of TRH to control rats only decreases the duration of LH pulses. However, in pituitary-grafted animals, TRH administration was followed by a decrease in the mean values of LH and in the absolute amplitude of the LH peaks. Vasoactive intestinal peptide (VIP) administration increased mean values of LH and the absolute and relative amplitudes of LH pulses in sham-operated animals, whereas only the relative amplitude of LH peaks was modified by VIP in pituitary-grafted rats. All these data suggest that hyperprolactinemia induced by pituitary-grafting interfere with the neuromodulator effects on the pulsatile regulatory center of the hypothalamus.
众所周知,促黄体生成素(LH)是以脉冲式方式释放的。然而,高催乳素血症对促黄体生成素(LH)脉冲性的影响尚未完全了解。本研究旨在描述高催乳素血症对LH脉冲性调节机制的影响。为此,通过将两个垂体移植到肾包膜下在雌性大鼠中诱导高催乳素血症。将年龄匹配的假手术动物用作对照。我们评估了两组动物中LH的脉冲模式。正如预期的那样,与对照动物的值相比,垂体移植增加了平均血清催乳素水平。促黄体生成素释放激素(LHRH)给药在对照或垂体移植大鼠中均未改变血清催乳素水平。促甲状腺激素释放激素(TRH)给药在两组中均增加了催乳素分泌。与对照大鼠相比,垂体移植大鼠中LH的平均值和LH峰值的绝对幅度增加。垂体移植未改变LH脉冲性的其他参数。给予LHRH后,LH释放增加,并且在对照大鼠中观察到第二次给予LHRH后的启动效应。与对照大鼠中观察到的反应相比,垂体移植动物中LH对LHRH给药的反应减弱。向对照大鼠给予两个TRH脉冲仅缩短了LH脉冲的持续时间。然而,在垂体移植动物中,给予TRH后LH的平均值和LH峰值的绝对幅度降低。血管活性肠肽(VIP)给药增加了假手术动物中LH的平均值以及LH脉冲的绝对和相对幅度,而在垂体移植大鼠中,VIP仅改变了LH峰值的相对幅度。所有这些数据表明,垂体移植诱导的高催乳素血症会干扰神经调节剂对下丘脑脉冲调节中心的作用。