Brooks V L, Blakemore L J
Department of Physiology, Oregon Health Sciences, University, Portland 97201.
Am J Physiol. 1989 Apr;256(4 Pt 1):E566-72. doi: 10.1152/ajpendo.1989.256.4.E566.
Vasopressin infusion has been shown to decrease plasma adrenocorticotropic hormone (ACTH) concentration and transiently increase plasma cortisol concentration in conscious dogs. In the present study, one experiment tested the hypothesis that vasopressin infusion decreases ACTH by activation of a V1 receptor mechanism, e.g., by increasing atrial pressures and stimulating the low-pressure baroreceptor reflex. Administration of a vasopressin V1 antagonist eliminated the increases in atrial pressure and decreases in heart rate with vasopressin infusion (1 ng.kg-1.min-1), as it eliminated the decrease in ACTH, which is consistent with baroreflex-mediated inhibition of ACTH by vasopressin. A second experiment evaluated the role of ACTH in the increase in glucocorticoids. Dexamethasone pretreatment, which inhibits ACTH secretion, abolished the increase in glucocorticoid concentration with vasopressin infusion, indicating that ACTH is necessary for the glucocorticoid response. A third experiment was performed to determine whether the glucocorticoid response could be restored in dexamethasone-treated dogs, when ACTH concentration was maintained near control levels by intravenous infusion of synthetic alpha-ACTH-(1-24) (0.3 ng.kg-1.min-1). In these dogs, vasopressin infusion produced a sustained increase in plasma glucocorticoid concentration from 22 +/- 3 to 49 +/- 8 ng/ml (P less than 0.001). Infusing higher levels of ACTH (0.5 ng.kg-1.min-1) enhanced basal glucocorticoid levels but did not enhance the response to vasopressin. Vasopressin infusion did not alter clearance of glucocorticoids. Collectively, these results suggest that vasopressin directly stimulates adrenal glucocorticoid production, provided that background levels of ACTH are present.
血管加压素输注已被证明可降低清醒犬的血浆促肾上腺皮质激素（ACTH）浓度，并使血浆皮质醇浓度短暂升高。在本研究中，一项实验检验了以下假设：血管加压素输注通过激活V1受体机制（例如，通过升高心房压力和刺激低压压力感受器反射）来降低ACTH。给予血管加压素V1拮抗剂可消除血管加压素输注（1 ng·kg⁻¹·min⁻¹）时心房压力的升高和心率的降低，因为它消除了ACTH的降低，这与血管加压素通过压力反射介导对ACTH的抑制作用一致。第二项实验评估了ACTH在糖皮质激素升高过程中的作用。地塞米松预处理可抑制ACTH分泌，它消除了血管加压素输注时糖皮质激素浓度的升高，表明ACTH是糖皮质激素反应所必需的。进行了第三项实验，以确定在通过静脉输注合成的α-ACTH-（1-24）（0.3 ng·kg⁻¹·min⁻¹）使ACTH浓度维持在接近对照水平的情况下，地塞米松处理的犬中糖皮质激素反应是否可以恢复。在这些犬中，血管加压素输注使血浆糖皮质激素浓度从22±3 ng/ml持续升高至49±8 ng/ml（P<0.001）。输注更高水平的ACTH（0.5 ng·kg⁻¹·min⁻¹）可提高基础糖皮质激素水平，但并未增强对血管加压素的反应。血管加压素输注未改变糖皮质激素的清除率。总体而言，这些结果表明，只要存在ACTH的背景水平，血管加压素就能直接刺激肾上腺糖皮质激素的产生。
