VASOACTIVE INTESTINAL POLYPEPTIDE EFFECTS A CENTRAL INHIBITION OF PULSATILE LUTEINIZING-HORMONE SECRETION IN OVARIECTOMIZED RATS
VASOACTIVE INTESTINAL POLYPEPTIDE EFFECTS A CENTRAL INHIBITION OF PULSATILE LUTEINIZING-HORMONE SECRETION IN OVARIECTOMIZED RATS
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DOI：
10.1210/endo-117-5-2134
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发表时间：
1985-01-01
期刊：
影响因子：
4.8
通讯作者：
STEINER, RA
中科院分区：
文献类型：
--
作者：
ALEXANDER, MJ;CLIFTON, DK;STEINER, RA
最近的研究表明，血管活性肠肽（VIP）作为一种神经递质或神经调质，一些观察表明，VIP，起源于大脑，可能会改变GnRH的分泌。我们已经测试的假设，VIP作为一个中枢神经系统调节器的脉冲式GnRH分泌，反映在脉冲式LH释放，通过评估的影响，脑室注射VIP对几个参数的LH分泌卵巢切除（OVX）大鼠。为了研究集中给药VIP改变垂体对GnRH反应的可能性，我们用GnRH挑战OVX大鼠，并比较VIP治疗动物与对照动物的LH反应。最后，我们测试的假设，即暴露的动物性腺类固醇改变VIP LH分泌的影响，通过评估LH释放VIP在OVX大鼠与雌激素和孕激素预处理的中央管理。未麻醉的大鼠与颈外静脉插管放血，在5分钟的时间间隔为2小时输注前和2小时，在连续脑室内输注VIP（1.8 nmol/h）或生理盐水。用等体积的血液置换混合物置换血液样品（300或400 μ l）。VIP输注使LH脉冲频率显著降低80%（P < 0.002），LH平均水平显著降低60%（P < 0.002），但对LH脉冲幅度无显著影响。相比之下，生理盐水输注对这些参数均无显著变化。血浆LH反应2 ng GnRH，静脉注射，在VIP治疗的动物没有显着差异，在对照组动物。最后，VIP输注对用苯甲酸雌二醇（50 μ g）和孕酮（25 mg）预处理的OVX大鼠的LH分泌没有可辨别的影响。这些结果表明，VIP可以深刻地抑制脉冲式LH分泌在OVX大鼠，并提供证据表明，这种影响是不是由于减少垂体对GnRH的反应。基于这些观察结果，我们认为，VIP，起源于脑内，可能是一个重要的抑制性调节器的脉动GnRH分泌。
Recent studies implicate vasoactive intestinal polypeptide (VIP) as a neurotransmitter or neuromodulator, and several observations suggest that VIP, originating within the brain, may alter the secretion of GnRH. We have tested the hypothesis that VIP acts as a central nervous system regulator of pulsatile GnRH secretion, as reflected in pulsatile LH release, by assessing the effect of intraventricularly administered VIP on several parameters of LH secretion in ovariectomized (OVX) rats. To examine the possibility that centrally administered VIP alters pituitary responsiveness to GnRH, we challenged OVX rats with GnRH and compared the LH response in VIP-treated animals with that in control animals. Finally, we tested the hypothesis that exposure of the animal to gonadal steroids alters VIPs effect on LH secretion by assessing LH release during central administration of VIP in OVX rats pretreated with estrogen and progesterone. Unanesthetized rats with external jugular cannulae were bled at 5-min intervals for 2 h before infusion and for 2 h during continuous intraventricular infusion of either VIP (1.8 nmol/h) or saline. Blood samples (300 or 400 .mu.l) were replaced with an equal volume of a blood replacement mixture. VIP infusion significantly reduced LH pulse frequency by 80% (P < 0.002) and mean LH levels by 60% (P < 0.002), but did not significantly affect LH pulse amplitude. In contrast, saline infusion produced no significant change in any of these parameters. The plasma LH response to 2 ng GnRH, iv, in VIP-treated animals did not differ significantly from that in control animals. Finally, VIP infusion had no discernible effect on LH secretion in OVX rats pretreated with estradiol benzoate (50 .mu.g) and progesterone (25 mg). These results demonstrate that VIP can profoundly inhibit pulsatile LH secretion in the OVX rat and provide evidence to suggest that this effect is not due to diminished pituitary responsiveness to GnRH. Based upon these observations, we argue that VIP, originating within the brain, may be an important inhibitory regulator of pulsatile GnRH secretion.