Woodland E, Tunny T J, Hamlet S M, Gordon R D
Clin Exp Pharmacol Physiol. 1985 May-Jun;12(3):245-8. doi: 10.1111/j.1440-1681.1985.tb02640.x.
Two males with glucocorticoid-suppressible hyperaldosteronism had hyperaldosteronism, hypertension and hypokalaemia corrected by continuous administration of physiological doses of dexamethasone for more than a year. During long-term dexamethasone treatment: (a) Plasma renin activity increased from subnormal to high normal levels, with normal posture-mediated increases; (b) Plasma aldosterone became responsive to angiotensin infusion, a new observation; (c) A fall in plasma aldosterone between 0800 h (recumbent) and 1000 h (upright) was replaced by a rise; (d) Plasma aldosterone became suppressible with salt loading. These findings are consistent with a shift to more normal control of aldosterone by renin-angiotensin, once abnormal responsiveness to ACTH has been nullified.
两名患有糖皮质激素可抑制性醛固酮增多症的男性,通过持续一年多给予生理剂量的地塞米松,其醛固酮增多症、高血压和低钾血症得到了纠正。在长期地塞米松治疗期间:(a)血浆肾素活性从低于正常水平升至正常高值水平,且体位介导的肾素活性增加正常;(b)血浆醛固酮对血管紧张素输注产生反应,这是一项新发现;(c)上午08:00(卧位)至10:00(立位)期间血浆醛固酮下降的情况被上升所取代;(d)盐负荷时血浆醛固酮可被抑制。一旦对促肾上腺皮质激素的异常反应被消除,这些发现与醛固酮的控制向更正常的肾素 - 血管紧张素调节转变是一致的。