Licorice-induced hypertension and syndromes of apparent mineralocorticoid excess.
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.
Walker
B R
BR
Department of Medicine, University of Edinburgh, Western General Hospital, Scotland, United Kingdom.
Edwards
C R
CR
D000312:Adrenal Hyperplasia, Congenital; D002229:Carbenoxolone / Q000009:adverse effects*; D006034:Glycyrrhetinic Acid / Q000009:adverse effects*; D006035:Glycyrrhiza / Q000737:chemistry; D006801:Humans; D006929:Hyperaldosteronism / Q000209:etiology*; D006973:Hypertension / Q000209:etiology*; D008901:Mineralocorticoids / Q000096:biosynthesis; D010946:Plants, Medicinal
D008901:Mineralocorticoids; D002229:Carbenoxolone; D006034:Glycyrrhetinic Acid