Graybeal M L, Fang V S, Landau R L
J Clin Endocrinol Metab. 1985 Oct;61(4):607-11. doi: 10.1210/jcem-61-4-607.
To assess the possible existence of a short loop feedback mechanism of direct glucocorticoid suppression on the adrenal glands, we performed a series of tests employing insulin hypoglycemia or ACTH infusions to obtain adrenal stimulation by ACTH levels that remained within the physiological range. Although the rapidity of glucocorticoid suppression of the pituitary thwarted efforts to use endogenous ACTH as a stimulus, we were able to mimic the stressed state by very low dose ACTH infusions (0.05 microgram/kg BW). No inhibition of cortisol secretion in response to ACTH infusions was detected in tests done after administration of dexamethasone compared to placebo [mean integrated response, 29.37 +/- 1.91 (+/- SE) vs. 29.12 +/- 1.12 microgram . h/dl, respectively]. Furthermore, when high doses of dexamethasone were administered iv, a small paradoxical increase in cortisol secretion was found (33.82 +/- 1.44 microgram . h/dl) without a difference in ACTH levels. These data do not support the concept of significant direct glucocorticoid inhibition of adrenal secretion. Non-ACTH factors that may enhance cortisol secretion in the presence of ACTH may exist.
为评估糖皮质激素对肾上腺直接抑制的短反馈机制的可能存在，我们进行了一系列试验，采用胰岛素低血糖或促肾上腺皮质激素（ACTH）输注，以通过保持在生理范围内的ACTH水平获得肾上腺刺激。尽管糖皮质激素对垂体抑制的快速性阻碍了使用内源性ACTH作为刺激物的尝试，但我们能够通过极低剂量的ACTH输注（0.05微克/千克体重）模拟应激状态。与安慰剂相比，在地塞米松给药后的试验中，未检测到对ACTH输注的皮质醇分泌抑制[平均综合反应分别为29.37±1.91（±标准误）对29.12±1.12微克·小时/分升]。此外，当静脉注射高剂量地塞米松时，发现皮质醇分泌有小的反常增加（33.82±1.44微克·小时/分升），而ACTH水平无差异。这些数据不支持糖皮质激素对肾上腺分泌有显著直接抑制的概念。可能存在在ACTH存在时可增强皮质醇分泌的非ACTH因素。
