Douglas A J, Johnstone H A, Wigger A, Landgraf R, Russell J A, Neumann I D
Department of Physiology, University Medical School, Edinburgh, UK.
J Endocrinol. 1998 Aug;158(2):285-93. doi: 10.1677/joe.0.1580285.
Endogenous opioid regulation of neurohypophysial and hypothalamo-pituitary-adrenal (HPA) axis hormone secretion in response to forced swimming (90 s in deep water at 19 degrees C) was investigated in virgin and 21-day-pregnant rats. There was no difference in basal plasma oxytocin concentrations between pregnant and virgin rats, but the opioid antagonist, naloxone, increased basal oxytocin secretion in the pregnant rats. Forced swimming increased oxytocin secretion similarly in pregnant and virgin rats, and this response was enhanced by naloxone. In pregnant rats naloxone had a greater effect (by 3.1-fold) than in virgins, showing stronger endogenous opioid restraint of an enhanced oxytocin secretory response to stress in pregnancy. Vasopressin secretion was not increased with forced swimming in virgin or pregnant rats, and naloxone had no effect. ACTH and corticosterone secretion in response to forced swimming was attenuated in pregnant rats compared to virgin rats, measured at 5 min. Naloxone had no effect on basal plasma ACTH or corticosterone concentration, but it reduced ACTH secretion in virgin rats 5 min after forced swimming; in pregnant rats naloxone had no such effect. Naloxone removed the pregnancy-related attenuation in corticosterone secretion measured at 5 min after forced swimming. Fifteen minutes after forced swimming, plasma corticosterone concentrations were not different between groups. In the late-pregnant rats, the increases in plasma ACTH and corticosterone induced by forced swimming were significantly prolonged compared to virgins. The results show that endogenous opioid inhibition emerges in pregnancy to restrict the responses of oxytocin neurones to a stressor. In contrast, the endogenous opioid enhancement of mechanisms regulating HPA axis secretory responses in virgin rats is not evident during pregnancy.
在未孕和妊娠21天的大鼠中，研究了内源性阿片类物质对神经垂体及下丘脑 - 垂体 - 肾上腺（HPA）轴激素分泌的调节作用，以应对强迫游泳（在19摄氏度深水中游泳90秒）。妊娠大鼠和未孕大鼠的基础血浆催产素浓度没有差异，但阿片类拮抗剂纳洛酮增加了妊娠大鼠的基础催产素分泌。强迫游泳使妊娠大鼠和未孕大鼠的催产素分泌同样增加，且这种反应被纳洛酮增强。在妊娠大鼠中，纳洛酮的作用（是未孕大鼠的3.1倍）比未孕大鼠更大，表明在妊娠期间，内源性阿片类物质对催产素对应激增强分泌反应的抑制作用更强。强迫游泳未使未孕或妊娠大鼠的血管加压素分泌增加，且纳洛酮对此无影响。在5分钟时测量发现，与未孕大鼠相比，强迫游泳后妊娠大鼠的促肾上腺皮质激素（ACTH）和皮质酮分泌减弱。纳洛酮对基础血浆ACTH或皮质酮浓度没有影响，但它降低了未孕大鼠强迫游泳后5分钟的ACTH分泌；在妊娠大鼠中，纳洛酮没有这种作用。纳洛酮消除了强迫游泳后5分钟时测量的与妊娠相关的皮质酮分泌减弱现象。强迫游泳15分钟后，各组之间的血浆皮质酮浓度没有差异。在妊娠晚期大鼠中，强迫游泳诱导的血浆ACTH和皮质酮增加比未孕大鼠显著延长。结果表明，妊娠期间出现内源性阿片类物质抑制作用，以限制催产素神经元对应激源的反应。相反，未孕大鼠中调节HPA轴分泌反应的内源性阿片类物质增强机制在妊娠期间并不明显。
