Inhibition of furosemide-induced kaliuresis in the rat by trilostane, an inhibitor of adrenal steroidogenesis
| Autor: | H.P. Schane, H. R. Harding, Gordon O. Potts, John E. Creange |
|---|---|
| Rok vydání: | 1984 |
| Předmět: |
Male
medicine.medical_specialty 3-Hydroxysteroid Dehydrogenases medicine.drug_class Natriuresis Trilostane Pharmacology Spironolactone General Biochemistry Genetics and Molecular Biology chemistry.chemical_compound Mineralocorticoid receptor Furosemide Internal medicine medicine Animals Aldosterone Adrenalectomy Dihydrotestosterone Rats Inbred Strains medicine.disease Hyperaldosteronism Diuresis Rats Endocrinology chemistry Mineralocorticoid Kaliuresis Potassium medicine.drug |
| Zdroj: | Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.). 177(3) |
| ISSN: | 0037-9727 |
| Popis: | In rats treated with furosemide, urinary losses of water, sodium and potassium were accompanied by increased circulating levels of aldosterone. Trilostane, an inhibitor of adrenal 3 beta-hydroxysteroid dehydrogenase activity, prevented furosemide-induced hyperaldosteronism which resulted in a partial inhibition of diuretic-induced kaliuresis without a change in sodium and water excretion. Spironolactone, an antagonist of mineralocorticoid action with inherent diuretic activity, produced qualitatively similar effects to those of trilostane on urinary electrolyte excretion in furosemide-treated intact rats. However, mineralocorticoid-induced potassium loss in adrenalectomized rats was not altered by trilostane but was prevented by spironolactone reflecting the direct effect of spironolactone on the kidney. In addition, furosemide-induced kaliuresis in adrenalectomized rats was not prevented by trilostane. Therefore, although both trilostane and spironolactone reduce diuretic-induced potassium loss, spironolactone acts by competing with aldosterone for the mineralocorticoid receptor while trilostane appears to act exclusively by preventing secondary hyperaldosteronism. |
| Databáze: | OpenAIRE |
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