Über das Verhalten von Renin und Aldosteron bei Patienten mit adrenaler Insuffizienz

Jungmann, E.; Magnet, W; Schöffling, Κ.

doi:10.1007/978-3-642-47091-2_352

Cited by 1 publication

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“…In this condition of steroid deficiency maximal elevated PRA levels are observed, which cannot be completely normalized by an adequate replacement therapy [19]. The renin release in adrenal insufficiency and during trilostane treatment is obviously not mediated through fl-adrenergic receptors or dependent upon renal prostaglandin synthesis but represents the direct answer of the juxtaglomerular apparatus to the depletion of sodium, potassium, and possibly arterial hypotension.…”

Section: Discussionmentioning

confidence: 95%

The inhibiting effect of trilostane on adrenal steroid synthesis: Hormonal and morphological alterations induced by subchronic trilostane treatment in normal rats

Jungmann

Magnet

et al. 1982

Res. Exp. Med.

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In adult male rats the effect of a subchronic treatment with trilostane, a new, orally active, competitive inhibitor of 3 beta-hydroxysteroid dehydrogenase, on adrenal steroid production and morphology was studied. Rats were treated with 150 mg or 300 mg trilostane/kg/day for 7 or 14 days and with 150 mg trilostane/kg/day for 10 days in combination with 75 mg propranolol/kg/day or 1 mg indomethacin/kg/day. Trilostane leads to a dose-dependent increase in adrenal weight and to a rather uniform increase in nuclear volumes of zona glomerulosa and zona fasciculata cells. The basal secretion of aldosterone and corticosterone is not significantly altered. Trilostane increases the excretion of sodium and potassium in urine. The stimulating effect of trilostane on plasma renin activity and the adrenal enlargement are not inhibited by propranolol or indomethacin. We conclude that trilostane induces latent adrenal insufficiency. Increased renin and ACTH maintain normal basal steroid levels, and might impair the therapeutic effectiveness of trilostane.

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Section: Discussionmentioning

confidence: 95%