Buckingham J C, Cooper T A
Neuroendocrinology. 1986;42(5):421-6. doi: 10.1159/000124481.
The influences of morphine and naloxone on hypothalamo-pituitary-adrenocortical (HPA) function were studied in the rat to investigate further the role of opioidergic mechanisms in the control of the secretion of corticotrophin and its hypothalamic releasing factor (CRF). Morphine not only caused rises in hypothalamic CRF content and plasma ACTH concentration but also potentiated the HPA response to stress. Its effects were antagonized by naloxone which, when given alone, did not influence basal plasma concentrations of ACTH and corticosterone but which inhibited, in a dose-dependent manner, the release of both of these hormones which normally occurs in response to stress. Naloxone also attenuated the exaggeration in stress-induced HPA activity but did not affect the increases in plasma ACTH concentration which followed adrenalectomy. The findings suggest that opioidergic mechanisms may be involved in the regulation of the HPA response to stress.
为了进一步研究阿片肽能机制在促肾上腺皮质激素及其下丘脑释放因子（CRF）分泌控制中的作用，在大鼠中研究了吗啡和纳洛酮对下丘脑 - 垂体 - 肾上腺皮质（HPA）功能的影响。吗啡不仅导致下丘脑CRF含量和血浆促肾上腺皮质激素（ACTH）浓度升高，还增强了HPA对应激的反应。其作用被纳洛酮拮抗，纳洛酮单独给药时不影响ACTH和皮质酮的基础血浆浓度，但以剂量依赖的方式抑制这两种激素通常在应激时的释放。纳洛酮还减弱了应激诱导的HPA活性的增强，但不影响肾上腺切除术后血浆ACTH浓度的升高。这些发现表明，阿片肽能机制可能参与了HPA对应激反应的调节。
