The GA constituent in licorice (and its metabolite 3-monoglucuronyl-glycyrrhetinic acid) inhibits the enzyme 11 HSD (Kato et al 1995), which catalyses the conversion of Cortisol into its inactive metabolite, cortisone. This results in delayed excretion and prolonged activity of Cortisol. Additionally, GL and GA bind to mineralocorticoid and glucocorticoid receptors and may displace Cortisol from its carrier molecule, transcortin (Nissen 2003).
Pseudohyperaldosteronism As Cortisol levels rise, they stimulate mineralocorticoid receptors in the distal renal tubule (Walker et al 1992). This creates pseudohyperaldosteronism, which has the same clinical features as primary aldosteronism, including sodium retention, fluid retention and oedema, hypertension, hypokalemia and metabolic alkalosis (Armanini et al 1996, Heldal & Midtvedt 2002, Kato et al 1995, vanUum et al 1998, Walker & Edwards 1994).
A case report suggests that the symptoms occur despite low plasma levels of aldosterone (Nobata et al 2001). Decreased plasma renin activity (Bernardi et al 1994, Epstein et al 1977) and increased Cortisol levels result in vasoconstriction of vascular smooth muscle (Dobbins & Saul 2000, Walker et al 1992), which may further exacerbate the hypertensive effects. This may be of particular significance in patients with prolonged intestinal transit time where GA levels can accumulate (Ploeger et al 2001).
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