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)