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Related Experiment Videos

Regulation of the 11 beta-hydroxysteroid dehydrogenase in the rat adrenal. Decrease enzymatic activity induced by

H Morita1, E N Cozza, M Y Zhou

  • 1Department of Internal Medicine, University of Missouri-Columbia 65201, USA.

Endocrine
|July 10, 1998
PubMed
Summary

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Adrenocorticotropic hormone (ACTH) inhibits 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta HSD-2) in rat adrenal cells. This inhibition increases the ratio of corticosterone to cortisone, contributing to ectopic ACTH syndrome symptoms.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Biochemistry

Background:

  • Ectopic ACTH syndrome causes hypertension and hypokalemic alkalosis due to increased cortisol/cortisone ratio.
  • This ratio change suggests inhibited 11 beta-hydroxysteroid dehydrogenase (11 beta HSD) activity.
  • Two 11 beta HSD isozymes exist; 11 beta HSD-2 is found in the rat adrenal cortex.

Purpose of the Study:

  • To investigate the effect of ACTH on 11 beta HSD-2 activity in rat adrenal cells.
  • To understand the mechanism by which ACTH influences mineralocorticoid receptor activity.

Main Methods:

  • Rat adrenal zona fasciculata (ZF) cells were dispersed and incubated with varying ACTH concentrations.
  • Corticosterone (B) and 11-dehydrocorticosterone (A) secretion was measured using ELISA.

Related Experiment Videos

  • Enzyme kinetics of [3H]B to [3H]A conversion in microsomes were analyzed with and without ACTH.

    • Main Results:

    • ACTH significantly increased the B/A ratio in ZF cells in a dose-dependent manner.
    • ACTH non-competitively inhibited 11 beta HSD-2 activity, reducing Vmax but not Km.
    • Dibutyryl cyclic AMP mimicked ACTH's effect, while calcium did not.

    Conclusions:

    • ACTH suppresses 11 beta HSD-2 activity in rat adrenal ZF cells via the ACTH receptor.
    • This noncompetitive inhibition leads to an increased B/A ratio, potentially explaining ectopic ACTH syndrome pathophysiology.
    • The findings highlight ACTH's role in regulating 11 beta HSD-2 activity and mineralocorticoid balance.