During a corticotropin-releasing hormone test in healthy subjects, administration of a beta-adrenergic antagonist induced secretion of cortisol and dehydroepiandrosterone sulfate and inhibited secretion of ACTH
During a corticotropin-releasing hormone test in healthy subjects, administration of a beta-adrenergic antagonist induced secretion of cortisol and dehydroepiandrosterone sulfate and inhibited secretion of ACTH
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DOI：
10.1530/eje.0.1480045
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发表时间：
2003-01-01
影响因子：
5.8
通讯作者：
Straub, RH
中科院分区：
文献类型：
--
作者：
Kizildere, S;Glück, T;Straub, RH
目的：在慢性炎症性疾病中，硫酸脱氢表雄酮（DHEA）（DHEAS）的血清水平较低。有趣的是，一些非炎症性疾病也表现出类似的低 DHEAS 水平，这表明存在其他抑制因素，例如交感神经系统 (SNS) 激活（例如心力衰竭、纤维肌痛或癌症恶病质患者）。我们的目的是确定 SNS 音调对 16 名男性和 12 名女性健康受试者刺激肾上腺类固醇分泌的影响。方法：一组在促肾上腺皮质激素释放激素 (CRII) 测试前 2 小时口服普萘洛尔，并测定促肾上腺皮质激素 (ACTH)、皮质醇、17-羟孕酮 (17OHP)、雄烯二酮、DHEA 和 DHEAS 的水平结果：普萘洛尔治疗可降低女性和男性受试者的心率（降低 20%）、舒张压（降低 20%）和血浆 ACTH，并增加血清皮质醇、血清 DHEAS 以及皮质醇/17OHP、皮质醇/DHEA 和 DHEAS/DHEA 的摩尔比。结论：β-肾上腺素能的影响似乎会降低与 ACTH 相关的 CRH 刺激的皮质醇和 17OHP，并降低与 DHEA 相关的 DHEAS。尽管其他研究人员发现β-肾上腺素能刺激培养的肾上腺皮质细胞中的类固醇分泌，但SNS通过β-肾上腺素受体的整体系统影响似乎在未刺激和刺激条件下抑制肾上腺类固醇。交感神经过度活跃可能是炎症和非炎症疾病中 DHEAS 水平低的共同点。
Objective: In chronic inflammatory diseases, serum levels of dehydroepiandrosterone (DHEA) sulfate (DHEAS) are low. Interestingly, several non-inflammatory diseases display similarly low levels of DHEAS which points to other inhibitory factors such as an activated sympathetic nervous system (SNS) (e.g. in patients with heart failure, fibromyalgia, or cancer cachexia). We aimed to identify the influence of the SNS tone on stimulated adrenal steroid secretion in 16 male and 12 female healthy subjects.Methods: One group were given oral propranolol 2 h before a corticotropin-releasing hormone (CRII) test, and levels of adrenocorticotropin (ACTH), cortisol, 17-hydroxyprogesterone (17OHP), androstenedione, DHEA, and DHEAS were measured.Results: Propranolol treatment decreased heart rate (by 20%), diastolic blood pressure (by 20%), and plasma ACTH, and increased serum cortisol, serum DHEAS, and the molar ratio of cortisol/17OHP, cortisol/DHEA, and DHEAS/DHEA similarly in female and male subjects.Conclusions: A beta-adrenergic influence seems to decrease CRH-stimulated cortisol in relation to ACTH and 17OHP, and decreases DHEAS in betarelation to DHEA. Although other workers have found beta-adrenergic stimulation of steroid secretion in cultured adrenocortical cells, the overall systemic influence of the SNS via beta-adrenoceptors seems to inhibit adrenal steroids under unstimulated and stimulated conditions. Sympathetic hyperactivity may be a common denominator for low levels of DHEAS in inflammatory and non-inflammatory diseases.