ROLE OF GLUCOCORTICOID IN EXCRETION OF AN ACUTE POTASSIUM LOAD IN PATIENTS WITH ADDISONS-DISEASE AND PANHYPOPITUITARISM

Glucocorticoid (GC) has been shown to stimulate potassium (K) excretio n 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 (panhypopituita rism) and with combined GC and mineralocorticoid deficiency (Addison's disease), studied 24 hours after withdrawal of their regular substitu tion therapy. Compared to data in healthy subjects, both basal K excre tion and the kaliuresis after a KCl load (1 mmol/kg body wt orally) we re impaired in either patient group (P < 0.05). Physiological cortisol supplementation (20 mg 3 hr prior to test, and 1 mg/hr during test) i ncreased basal K excretion (from 10.6 +/- 1.8 to 19.2 +/- 1.9 mmol/5 h r, 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. C ortisol 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, altho ugh KCl-stimulated K excretion remained below normal (P < 0.01). The e ffects of cortisol on sodium excretion differed between the two patien t groups (P < 0.05) in that only in Addison's disease the improved K e xcretion 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 als o improved K excretion (P < 0.05), but without the concomitant sodium retention observed after cortisol. These data speak for a physiologica l role of GC in potassium homeostasis, and also suggest that cortisol, as the important endogenous GC hormone, has mineralocorticoid-like ef fects specifically in the absence of aldosterone.