Schambelan M, Brust N L, Chang B C, Slater K L, Biglieri E G
J Clin Endocrinol Metab. 1976 Jul;43(1):115-31. doi: 10.1210/jcem-43-1-115.
The effect of circadian rhythm and alterations in posture on plasma aldosterone concentration was studied in 13 patients with primary aldosteronism (six adenoma, five idiopathic hyperplasia, two carcinoma) to define the regulatory mechanism in each of these pathologic subtypes. Blood samples for aldosterone, cortisol, renin, and potassium concentrations were obtained every 4 h during prolonged recumbency (32 h) and upright posture (16 h). During recumbency, aldosterone and cortisol followed a normal circadian pattern in patients with adenoma and hyperplasia, with peak values at 0400-0800 h and the nadir at 1600-2400 h. Normalized aldosterone and cortisol values correlated significantly in both groups (adenoma r=+0.66, P less than 0.001; hyperplasia r=+0.42, P less than 0.01). With upright posture, aldosterone levels declined parallel to the normal circadian fall in cortisol in patients with adenoma (r=+0.68, P less than 0.001); whereas aldosterone levels increased in patients with hyperplasia parallel to small increments in renin (r=+0.65, P less than 0.001) and potassium (r=+0.64, P less than 0.001). During the administration of dexamethasone, aldosterone no longer correlated with cortisol in patients with adenoma but continued to correlate with renin during upright studies in patients with hyperplasia (r=+0.77, P less than 0.01). Aldosterone circadian rhythm was abnormal in patients with carcinoma and no effect of posture was noted. Unilateral adrenalectomy restored the normal postural relationship in four patients with adenoma. These studies suggest that aldosterone secretion is under continuous ACTH control regardless of posture in patients with adenoma, whereas persistent adrenal responsiveness to small increments in renin and/or potassium mediate the postural increase in plasma aldosterone in patients with hyperplasia. True adrenal autonomy occurs only in patients with adrenal carcinoma and when ACTH is suppressed in those with adenoma.
对13例原发性醛固酮增多症患者(6例腺瘤、5例特发性增生、2例癌)研究了昼夜节律和姿势改变对血浆醛固酮浓度的影响,以明确每种病理亚型的调节机制。在长时间卧位(32小时)和直立姿势(16小时)期间,每4小时采集一次血样检测醛固酮、皮质醇、肾素和钾浓度。卧位时,腺瘤和增生患者的醛固酮和皮质醇呈现正常的昼夜模式,峰值在0400 - 0800时,最低点在1600 - 2400时。两组中醛固酮和皮质醇的标准化值均显著相关(腺瘤组r = +0.66,P < 0.001;增生组r = +0.42,P < 0.01)。直立姿势时,腺瘤患者的醛固酮水平与皮质醇正常的昼夜下降平行下降(r = +0.68,P < 0.001);而增生患者的醛固酮水平随肾素(r = +0.65,P < 0.001)和钾(r = +0.64,P < 0.001)的小幅升高而升高。地塞米松给药期间,腺瘤患者的醛固酮不再与皮质醇相关,但增生患者在直立研究期间醛固酮仍与肾素相关(r = +0.77,P < 0.01)。癌患者的醛固酮昼夜节律异常,未观察到姿势的影响。单侧肾上腺切除术恢复了4例腺瘤患者的正常姿势关系。这些研究表明,腺瘤患者无论姿势如何,醛固酮分泌均受持续的促肾上腺皮质激素控制,而增生患者中肾素和/或钾的小幅升高引起的肾上腺持续反应性介导了血浆醛固酮的姿势性升高。真正的肾上腺自主性仅发生在肾上腺癌患者以及腺瘤患者中促肾上腺皮质激素被抑制时。