Etomidate suppresses adrenocortical function by inhibition of 11 beta-hydroxylation

Abstract

We studied the effect of short term infusion of the imidazole-derived anesthetic agent etomidate on plasma concentrations of ACTH, cortisol, and the cortisol-precursors 11-desoxycortisol and 17-hydroxyprogesterone. During the infusion of etomidate, a significant increase in the peripheral concentration of ACTH occurred, while plasma cortisol concentrations decreased. After the end of the infusion, cortisol concentrations further decreased, while the concentrations of desoxycortisol and 17-hydroxyprogesterone increased. Furthermore, in in vitro experiments with isolated rat pituitary and adrenal cells, etomidate did not affect corticotropin-releasing hormone-induced ACTH secretion from pituitary cells, whereas ACTH-stimulated corticosterone secretion from adrenal cells was inhibited by addition of etomidate in concentrations which occur in plasma during and after infusion of the drug. These results lead to the conclusion that etomidate inhibits adrenal 11 beta-hydroxylation.