Licorice-induced hypertension and syndromes of apparent mineralocorticoid excess

Endocrinol Metab Clin North Am. 1994 Jun;23(2):359-77.


Excessive ingestion of licorice induces a syndrome of hypokalemia and hypertension that reflects increased activation of renal mineralocorticoid receptors by cortisol. A similar syndrome of cortisol-dependent mineralocorticoid excess occurs in congenital deficiency of the enzyme 11 beta-hydroxysteroid dehydrogenase, which normally inactivates cortisol to cortisone. It has been shown that licorice inhibits 11 beta-dehydrogenase, preventing local inactivation of cortisol and allowing cortisol inappropriate access to intrinsically nonspecific renal mineralocorticoid receptors. Further studies with licorice and its derivatives have revealed a widespread role for 11 beta-dehydrogenase in regulating tissue sensitivity to cortisol. Deficient 11 beta-dehydrogenase activity provides a novel pathogenetic mechanism for hypertension, and current research suggests that several common forms of hypertension can be explained by the mechanisms that operate in licorice-induced hypertension.

Publication types

  • Review

MeSH terms

  • Adrenal Hyperplasia, Congenital
  • Carbenoxolone / adverse effects*
  • Glycyrrhetinic Acid / adverse effects*
  • Glycyrrhiza* / chemistry
  • Humans
  • Hyperaldosteronism / etiology*
  • Hypertension / etiology*
  • Mineralocorticoids / biosynthesis
  • Plants, Medicinal*


  • Mineralocorticoids
  • Carbenoxolone
  • Glycyrrhetinic Acid