Hyperaldosteronism in the sodium-depleted rat: Mode of aldosterone-stimulating action of frusemide

A. Spät, E. Tarjan, G. Toth

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

The mechanism of diuretic-induced hyperaldosteronism was examined in dexamethasone-pretreated rats. The diuretic drug frusemide brought about a rapid increase in plasma renin activity and aldosterone concentration in serum. Half an hour after the administration of frusemide the mean concentration of aldosterone was 25 times higher than in vehicle-treated control animals. Administration of SQ 20,881, an inhibitor of angiotensin converting enzyme, prevented the adrenal response to frusemide. The response of aldosterone was completely blocked by indomethacin. This drug reduced renin release and probably also inhibited the effect on the adrenal glands of angiotensin, released in response to frusemide. Our results indicate that the effects of diuretics on the adrenal glomerulosa cells are mediated by the renin-angiotensin system also in the rat. Hyperaldosteronism is dependent on the maintenance of prostaglandin synthesis. ACTH has no essential role in this response.

Original languageEnglish
Pages (from-to)7-15
Number of pages9
JournalJournal of Endocrinology
Volume82
Issue number1
Publication statusPublished - 1979

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Hyperaldosteronism
Furosemide
Aldosterone
Sodium
Diuretics
Renin
Zona Glomerulosa
Angiotensins
Renin-Angiotensin System
Adrenal Glands
Angiotensin-Converting Enzyme Inhibitors
Indomethacin
Pharmaceutical Preparations
Adrenocorticotropic Hormone
Dexamethasone
Prostaglandins
Maintenance
Serum

ASJC Scopus subject areas

  • Endocrinology

Cite this

Hyperaldosteronism in the sodium-depleted rat : Mode of aldosterone-stimulating action of frusemide. / Spät, A.; Tarjan, E.; Toth, G.

In: Journal of Endocrinology, Vol. 82, No. 1, 1979, p. 7-15.

Research output: Contribution to journalArticle

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