van Buren M, Rabelink T J, Koppeschaar H P, Koomans H A
Department of Nephrology & Hypertension, and Endocrinology, University Hospital Utrecht, The Netherlands.
Kidney Int. 1993 Nov;44(5):1130-8. doi: 10.1038/ki.1993.359.
Glucocorticoid (GC) has been shown to stimulate potassium (K) excretion in various conditions, but it is still incompletely resolved whether its presence is essential for the normal K homeostasis. We addressed this question in patients with selective GC deficiency (panhypopituitarism) and with combined GC and mineralocorticoid deficiency (Addison's disease), studied 24 hours after withdrawal of their regular substitution therapy. Compared to data in healthy subjects, both basal K excretion and the kaliuresis after a KCl load (1 mmol/kg body wt orally) were impaired in either patient group (P < 0.05). Physiological cortisol supplementation (20 mg 3 hr prior to test, and 1 mg/hr during test) increased basal K excretion (from 10.6 +/- 1.8 to 19.2 +/- 1.9 mmol/5 hr, P < 0.01) and KCl stimulated kaliuresis (from 47.9 +/- 6.1 to 54.8 +/- 4.7 mmol/5 hr, P = 0.06) to normal levels in panhypopituitarism. Cortisol also improved basal K excretion (from 10.2 +/- 1.5 to 16.9 +/- 3.5 mmol/5 hr, P < 0.05) and KCl-stimulated K excretion (from 31.6 +/- 2.5 to 45.2 +/- 3.8 mmol/5 hr, P < 0.05) in Addison's disease, although KCl-stimulated K excretion remained below normal (P < 0.01). The effects of cortisol on sodium excretion differed between the two patient groups (P < 0.05) in that only in Addison's disease the improved K excretion was associated with sodium retention. Additional experiments with the purely GC compound dexamethasone (0.5 mg 3 hr prior to test, and 0.03 mg/hr during test) in the patients with Addison's disease also improved K excretion (P < 0.05), but without the concomitant sodium retention observed after cortisol.(ABSTRACT TRUNCATED AT 250 WORDS)
糖皮质激素（GC）已被证明在各种情况下均可刺激钾（K）排泄，但它对于正常钾稳态是否必不可少仍未完全明确。我们在选择性GC缺乏（全垂体功能减退症）患者以及GC和盐皮质激素联合缺乏（艾迪生病）患者中解决了这个问题，这些患者在停止常规替代治疗24小时后接受研究。与健康受试者的数据相比，两组患者的基础钾排泄以及氯化钾负荷（口服1 mmol/kg体重）后的尿钾排泄均受损（P<0.05）。生理性补充皮质醇（测试前3小时20 mg，测试期间1 mg/小时）可使全垂体功能减退症患者的基础钾排泄（从10.6±1.8增加至19.2±1.9 mmol/5小时，P<0.01）以及氯化钾刺激的尿钾排泄（从47.9±6.1增加至54.8±4.7 mmol/5小时，P = 0.06）提高至正常水平。皮质醇也改善了艾迪生病患者的基础钾排泄（从10.2±1.5增加至16.9±3.5 mmol/5小时，P<0.05）以及氯化钾刺激的钾排泄（从31.6±2.5增加至45.2±3.8 mmol/5小时，P<0.05），尽管氯化钾刺激的钾排泄仍低于正常水平（P<0.01）。皮质醇对钠排泄的影响在两组患者之间存在差异（P<0.05），因为仅在艾迪生病中，改善的钾排泄与钠潴留相关。在艾迪生病患者中使用纯GC化合物地塞米松（测试前3小时0.5 mg，测试期间0.03 mg/小时）进行的额外实验也改善了钾排泄（P<0.05），但没有观察到皮质醇后伴随的钠潴留。（摘要截断于250字）
