Oberfield S E, Levine L S, Stoner E, Chow D, Rauh W, Greig F, Lee S M, Lightner E, Witte M, New M I
J Clin Endocrinol Metab. 1981 Jul;53(1):158-64. doi: 10.1210/jcem-53-1-158.
The response of the adrenal glomerulosa to renin stimulation was determined in 10 patients with dexamethasone-suppressible hyperaldosteronism. The patients were treated continuously with 2 mg/day dexamethasone (DEX) and were studied on a regular sodium diet (87 meq/m2 . day) and on a 10 meq/day sodium diet. With DEX treatment all patients showed a prompt suppression of adrenal fasciculata function as evidenced by suppression of serum cortisol, corticosterone, desoxycorticosterone, and urinary 18-OH-desoxycorticosterone. The complete suppression of urinary pH 1 aldosterone (aldo) by DEX, unique to this disorder, was paralleled by a prompt suppression of urinary 18-OH-corticosterone. With continued DEX administration, plasma renin activity rose to the normal or supranormal range. Dietary sodium restriction resulted in a further rise in plasma renin activity and a rise in urinary pH 1 aldo and 18-OH-corticosterone. We conclude that in DEX-suppressible hyperpaldosteronism, although ACTH appears to be the primary stimulus for aldo secretion in the untreated state, when ACTH is suppressed, the adrenal glomerulosa responds normally to the stimulation of renin-angiotensin II.
在10例地塞米松可抑制性醛固酮增多症患者中，测定了肾上腺球状带对肾素刺激的反应。患者持续接受2mg/天的地塞米松（DEX）治疗，并在常规钠饮食（87meq/m²·天）和10meq/天的钠饮食条件下进行研究。接受DEX治疗时，所有患者的肾上腺束状带功能均迅速受到抑制，血清皮质醇、皮质酮、脱氧皮质酮和尿18-羟基脱氧皮质酮水平降低可证明这一点。DEX对尿pH1醛固酮（aldo）的完全抑制是这种疾病所特有的，同时尿18-羟基皮质酮也迅速受到抑制。持续给予DEX时，血浆肾素活性升至正常或超正常范围。饮食中钠的限制导致血浆肾素活性进一步升高，尿pH1aldo和18-羟基皮质酮升高。我们得出结论，在地塞米松可抑制性醛固酮增多症中，虽然在未治疗状态下促肾上腺皮质激素似乎是醛固酮分泌的主要刺激因素，但当促肾上腺皮质激素受到抑制时，肾上腺球状带对肾素-血管紧张素II的刺激反应正常。
