Effects of corticosteroids on urinary ammonium excretion in humans

This study was designed to examine the selective effects of glucocorticoid and mineralocorticoid classes of steroid hormones on urinary ammonium excretion in humans. In 22 10-day studies, normal male volunteers received either 9 alpha-fludrohydrocortisone or hydrocortisone, alone or with the recepto...

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Bibliographic Details
Published in:Journal of the American Society of Nephrology 1994-02, Vol.4 (8), p.1531-1537
Main Authors: Waybill, M M, Clore, J N, Emerick, R A, Watlington, C O, Schoolwerth, A C
Format: Article
Language:English
Subjects:
Adult
Chlorides - urine
Diuresis - drug effects
Fludrocortisone - pharmacology
Humans
Hydrocortisone - pharmacology
Hydrogen-Ion Concentration
Male
Mineralocorticoid Receptor Antagonists
Potassium - urine
Quaternary Ammonium Compounds - urine
Receptors, Glucocorticoid - antagonists & inhibitors
Receptors, Glucocorticoid - physiology
Receptors, Mineralocorticoid - physiology
Spironolactone - pharmacology
Water-Electrolyte Balance - physiology
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Summary:This study was designed to examine the selective effects of glucocorticoid and mineralocorticoid classes of steroid hormones on urinary ammonium excretion in humans. In 22 10-day studies, normal male volunteers received either 9 alpha-fludrohydrocortisone or hydrocortisone, alone or with the receptor antagonist spironolactone or mifepristone. The small but significant increase in ammonium excretion noted with the administration of 9 alpha-fludrohydrocortisone was associated with a significant decrease in serum potassium. In contrast, a significantly larger increase in ammonium excretion was noted with hydrocortisone, without concomitant electrolyte changes. Spironolactone did not alter the effect on ammonium excretion by either corticosteroid, whereas mifepristone markedly blunted the hydrocortisone-induced increase in urinary ammonium excretion. It was concluded that glucocorticoids increase urinary ammonium excretion in humans and that this effect occurs through binding to the Type II (glucocorticoid) receptor rather than by cross-occupancy of the Type I (mineralocorticoid) receptor.
ISSN:1046-6673
DOI:10.1681/ASN.V481531