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首页> 外文期刊>American Journal of Physiology >Interaction of PGHS-2 and glutamatergic mechanisms controlling the ovine fetal hypothalamus-pituitary-adrenal axis.
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Interaction of PGHS-2 and glutamatergic mechanisms controlling the ovine fetal hypothalamus-pituitary-adrenal axis.

机译：PGHS-2和谷氨酸机制控制绵羊胎儿垂体肾上腺轴的相互作用。

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Prostaglandins, generated within the fetal brain, are integral components of the mechanism controlling the fetal hypothalamus-pituitary-adrenal (HPA) axis. Previous studies in this laboratory demonstrated that prostaglandin G/H synthase isozyme 2 (PGHS-2) inhibition reduces the fetal HPA axis response to cerebral hypoperfusion, blocks the preparturient rise in fetal plasma ACTH concentration, and delays parturition. We also discovered that blockade of N-methyl-d-aspartate (NMDA) receptors reduces the fetal ACTH response to cerebral hypoperfusion. The present study was designed to test the hypothesis that PGHS-2 action and the downstream effect of HPA axis stimulation are stimulated by NMDA-mediated glutamatergic neurotransmission. Chronically catheterized late-gestation fetal sheep (n = 8) were injected with NMDA (1 mg iv). All responded with increases in fetal plasma ACTH and cortisol concentrations. Pretreatment with resveratrol (100 mg iv, n = 5), a specific inhibitor of PGHS-1, did not alter the magnitude of the HPA axis response to NMDA. Pretreatment with nimesulide (10 mg iv, n = 6), a specific inhibitor of PGHS-2, significantly reduced the HPA axis response to NMDA. To further explore this interaction, we injected NMDA in six chronically catheterized fetal sheep that were chronically infused with nimesulide (n = 6) at a rate of 1 mg/day into the lateral cerebral ventricle for 5-7 days. In this group, there was no significant ACTH response to NMDA. Finally, we tested whether the HPA axis response to prostaglandin E(2) (PGE(2)) is mediated by NMDA receptors. Seven chronically catheterized late-gestation fetal sheep were injected with 100 ng of PGE(2), which significantly increased fetal plasma ACTH and cortisol concentrations. Pretreatment with ketamine (10 mg iv), an NMDA antagonist, did not alter the ACTH or cortisol response to PGE(2). We conclude that generation of prostanoids via the action of PGHS-2 in the fetal brain augments the fetal HPA axis response to NMDA-mediated glutamatergic stimulation.
机译：在胎儿脑内产生的前列腺素是控制胎儿下丘脑 - 垂体肾上腺（HPA）轴的机制的组成部分。此实验室的先前研究表明，前列腺素G / H合酶同工酶2（PGHS-2）抑制减少了对脑低血量灌注的胎儿HPA轴响应，阻断胎儿血浆诱变的预备分管升高，延迟分娩。我们还发现，封闭的N-甲基-D-天冬氨酸（NMDA）受体降低了对脑低血量灌注的胎儿acth反应。本研究旨在测试PGHS-2动作和HPA轴刺激的下游效果的假设由NMDA介导的谷氨酸谷氨酸神经递质刺激。将慢性导管插入的晚期妊娠胎儿绵（n = 8）注射NMDA（1mg IV）。所有反应胎儿血浆ActH和皮质醇浓度的增加。与白藜芦醇（100mg IV，N = 5）的预处理，PGHS-1的特异性抑制剂，没有改变HPA轴对NMDA的响应的大小。用Nimesulide（10mg IV，N = 6）的预处理是PGHS-2的特异性抑制剂，显着降低了对NMDA的HPA轴响应。为了进一步探索这种相互作用，我们在六个慢性导管胎儿绵羊中注射NMDA，其以1mg /天的速率慢慢地注入南侧脑室5-7天。在该组中，对NMDA没有明显的acth响应。最后，我们测试了对前列腺素E（2）（PGE（2））的HPA轴响应是否由NMDA受体介导。将七个慢性导管直肠妊娠胎儿注射100 ng PGE（2），这显着增加了胎儿血浆ACTH和皮质醇浓度。用氯胺酮（10mg IV），NMDA拮抗剂的预处理没有改变acth或皮质醇对PGE（2）的反应。我们得出结论，通过PGHS-2在胎儿脑中的作用产生前列腺醇的产生增加了胎儿HPA轴对NMDA介导的谷氨酸胶刺激的反应。

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