Role of glucocorticoid in excretion of an acute potassium load in patients with Addison's disease and panhypopituitarism

Abstract

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. These data speak for a physiological role of GC in potassium homeostasis, and also suggest that cortisol, as the important endogenous GC hormone, has mineralocorticoid-like effects specifically in the absence of aldosterone.