Bugajski J
Department of Physiology, Polish Academy of Sciences, Cracow, Poland.
J Physiol Pharmacol. 1996 Dec;47(4):559-75.
Role of the prostaglandins (PGs) in the activation of the hypothalamic-pituitary-adrenal (HPA) axis by the adrenergic agonists, corticotropin-releasing hormone (CRH) and vasopressin (VP) in rats under basal and social stress conditions was investigated. Systemic or intracerebroventricular (icv) pretreatment with indomethacin powerfully reduced the corticosterone response to ivc phenylephrine, and alpha 1-receptor agonist, significantly diminished the response to clonidine, an alpha 2-receptor agonist, but did not alter the response to isoprenaline, a beta-adrenergic agonist. Consequently, indomethacin considerably reduced the corticosterone response to noradrenaline, and alpha 1- and alpha 2-adrenergic agonist, but did not change the response to adrenaline, a predominant beta-adrenergic agonist. Thus, prostaglandins considerably mediate the HPA activity stimulated via central alpha 1- and alpha 2- but not beta-adrenergic receptors. Social crowding stress for 3 days did not affect the corticosterone response to ip or icv CRH, but drastically reduced the response to VP. In stressed rats indomethacin did not alter the corticosterone response to CRH but significantly further impaired the diminished by stress corticosterone response to VP. Neither social stress nor endogenous prostaglandins affected the responsiveness of the CRH system. By contrast, both social stress and prostaglandins considerably diminished the HPA response to VP. The above results indicate that both these neurohormone systems have a distinct mode of adaptation and interaction with PG systems during social stress. Interleukins, particularly IL-1 beta and IL-6, activate the HPA axis. Most immunological stimuli and interleukins also activate both the central and the peripheral noradrenergic systems. Activation of the HPA axis in vivo depends on the secretion of CRH, an intact pituitary and the ventral adrenergic bundle innervating the hypothalamic paraventricular nucleus. Interleukins may cross the blood-brain-barrier or be produced in the CNS to stimulate their receptors in brain structures involved in the regulation of the HPA axis.
研究了前列腺素（PGs）在基础和社会应激条件下对大鼠肾上腺素能激动剂、促肾上腺皮质激素释放激素（CRH）和血管加压素（VP）激活下丘脑-垂体-肾上腺（HPA）轴中的作用。用吲哚美辛进行全身或脑室内（icv）预处理可显著降低皮质酮对静脉注射去氧肾上腺素（一种α1受体激动剂）的反应，显著减弱对可乐定（一种α2受体激动剂）的反应，但不改变对异丙肾上腺素（一种β肾上腺素能激动剂）的反应。因此，吲哚美辛显著降低了皮质酮对去甲肾上腺素（一种α1和α2肾上腺素能激动剂）的反应，但不改变对肾上腺素（一种主要的β肾上腺素能激动剂）的反应。因此，前列腺素显著介导通过中枢α1和α2肾上腺素能受体而非β肾上腺素能受体刺激的HPA活性。3天的社会拥挤应激不影响皮质酮对腹腔注射或脑室内注射CRH的反应，但显著降低对VP的反应。在应激大鼠中，吲哚美辛不改变皮质酮对CRH的反应，但显著进一步损害了应激导致的皮质酮对VP反应的减弱。社会应激和内源性前列腺素均不影响CRH系统的反应性。相比之下，社会应激和前列腺素均显著减弱了HPA对VP的反应。上述结果表明，在社会应激期间，这两种神经激素系统与PG系统具有不同的适应模式和相互作用。白细胞介素，特别是IL-1β和IL-6，激活HPA轴。大多数免疫刺激和白细胞介素也激活中枢和外周去甲肾上腺素能系统。体内HPA轴的激活取决于CRH的分泌、完整的垂体以及支配下丘脑室旁核的腹侧肾上腺素能束。白细胞介素可能穿过血脑屏障或在中枢神经系统中产生，以刺激参与HPA轴调节的脑结构中的受体。
