Mantero F, Armanini D, Boscaro M
Horm Metab Res. 1978 Jan;10(1):65-71. doi: 10.1055/s-0028-1093484.
The renin-angiotensin-aldosterone system has been evaluated in 19 patients with Cushing's syndrome due to bilateral adrenal hyperplasia and in 2 patients with unilateral adenoma. In the first group urinary aldosterone was within the normal limits with a mean of 8.3 +/- 1.86 microgram/24 h. Aldosterone excretion did not change significantly after furosemide administration, ACTH infusion or dexamethasone. Upright PRA was suppressed in 9/16 patients with a mean of 4.9 +/- 1.85 ng/ml/3 h and showed only a slight response to furosemide. Dexamethasone alone did not produce any change. Both aldosterone and PRA were to some extent stimulated by an association of dexamethasone and furosemide. In the 2 patients with adenoma, aldosterone excretion was also normal, but PRA was very elevated. From our data it is concluded that in Cushing's syndrome due to bilateral hyperplasia, PRA and aldosterone excretion are partially suppressed. From our results on plasma deoxycorticosterone and corticosterone concentration it seems unlikely that these mineralocorticoids are the major cause of this phenomenon. However, it may not be excluded that other yet unidentified hormones could play some role in the pathogenesis of hypertension and renin suppression in Cushing's syndrome.
对19例因双侧肾上腺增生所致库欣综合征患者及2例单侧腺瘤患者的肾素-血管紧张素-醛固酮系统进行了评估。在第一组中,尿醛固酮在正常范围内,平均为8.3±1.86微克/24小时。给予速尿、促肾上腺皮质激素(ACTH)输注或地塞米松后,醛固酮排泄无明显变化。16例患者中有9例立位血浆肾素活性(PRA)受到抑制,平均为4.9±1.85纳克/毫升/3小时,对速尿仅表现出轻微反应。单独使用地塞米松未产生任何变化。地塞米松和速尿联合使用在一定程度上刺激了醛固酮和PRA。在2例腺瘤患者中,醛固酮排泄也正常,但PRA非常升高。根据我们的数据得出结论,在双侧增生所致的库欣综合征中,PRA和醛固酮排泄部分受到抑制。从我们关于血浆脱氧皮质酮和皮质酮浓度的结果来看,这些盐皮质激素似乎不太可能是这种现象的主要原因。然而,不能排除其他尚未确定的激素可能在库欣综合征高血压和肾素抑制的发病机制中起一定作用。