18-Oxocortisol: Effect of dexamethasone, ACTH and sodium restriction

Celso E. Gomez-Sanchez, Philip G. Zager, Mark F. Foecking, O. Bryan Holland, Arunabha Ganguly

Research output: Contribution to journalArticlepeer-review

9 Scopus citations

Abstract

The urinary excretion of 18-oxocortisol in 37 normal subjects consuming a normal sodium diet was 1.2 ± 0.9(SD) μg/24h. Dexamethasone administration to 5 normal individuals suppressed the excretion of 18-oxocortisol from 1.16 ± 0.5 μm/24h to 0.6 ± 0.2 μg/24h. While they still received dexamethasone, ACTH administration raised the 18-oxo-cortisol excretion to 3.82 ± 1.2 μg/24h. Seven normal subjects were placed on a sodium restricted diet, and the urinary excretion of 18-oxocortisol rose from 1.5 ± 1.21 μg/24h to 8.54 ± 5.08 μg/24h and aldosterone from 6.6 ± 2.0 μg/24h to 39.7 ± 14.6 μg/24h. Two of the seven individuals showed minimal increases in the excretion of 18-oxocortisol, but in all cases aldosterone increased with sodium restriction. The urinary excretion of 18-oxocortisol correlated significantly with the excretion of aldosterone, 18-hydroxycortisol, cortisol, and 19-nordeoxycorticosterone. These studies indicate that 18-oxocortisol secretion is under ACTH regulation, but since sodium restriction also increases the excretion of 18-oxocortisol, the renin-angiotensin system must also participate in its regulation. However, some individuals do not increase their excretion of 18-oxocortisol with sodium restriction, although aldosterone excretion increases as expected, suggesting that additional factors participate in the regulation of 18-oxocortisol production.

Original languageEnglish (US)
Pages (from-to)409-412
Number of pages4
JournalJournal of Steroid Biochemistry
Volume32
Issue number3
DOIs
StatePublished - Mar 1989

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology

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