Liquorice-induced rise in blood pressure: a linear dose-response relationship

Abstract

To clarify the dose-response and the time-response relationship between liquorice consumption and rise in blood pressure and explore the inter-individual variance this intervention study was designed and executed in research laboratories at University hospitals in Iceland and Sweden. Healthy, Caucasian volunteers who also served as a control for himself/herself consumed liquorice in various doses, 50-200 g/day, for 2-4 weeks, corresponding to a daily intake of 75-540 mg glycyrrhetinic acid, the active substance in liquorice. Blood pressure was measured before, during and after liquorice consumption. Systolic blood pressure increased by 3.1-14.4 mm Hg (P Ͻ 0.05 for all), demonstrating a dose-

Endothelin 1 Type A Receptor Antagonism Prevents Vascular Dysfunction and Hypertension Induced by 11β-Hydroxysteroid Dehydrogenase Inhibition: Role of Nitric Oxide

“…Moreover, I have treated a few patients with AME, and it has proved impossible to normalize BP with antihypertensive agents other than the mineralocorticoid receptor antagonist spironolactone. 3 However, verapamil and LU135252 normalized BP in GA-treated rats in this study. 1 Considering the mechanism of BP elevation associated with inhibited 11␤HSD2 activity, these results are questionable.…”

“…1 The changes we see after GAT treatment are exactly as expected and are in complete agreement with recent reports of liquorice-induced hypertension in man. 2,3 Regarding Dr Ferrari's findings in a few apparent mineralocorticoid excess (AME) patients, we see nothing inconsistent with the idea that GA-induced hypertension in rats may well involve components that are sensitive to verapamil and endothelin antagonists. Finally, in this paper, we do not claim to have analyzed the detailed mechanisms of GA-induced alterations in the endothelin system.…”

“…2 This prevents blood pressure (BP) increases associated with excess renal sodium reabsorption. 2,3 With reduced 11␤HSD2 activity, as observed with the genetic defect called apparent mineralocorticoid excess (AME) syndrome or with inhibition by glycyrrhetinic acid (GA), the active liquorice component is signaled by a relative deficiency of 11-ketoglucocorticoids. This is detected by an increased urinary ratio of active to inactive tetrahydro-(TH-) glucocorticoids.…”

“…3 In AME syndrome, the (THFϩ5␣THF)/THE ratios are increased to 20 to 50, as compared with normal values of 0.75 to 1.25. 3 Ruschitzka et al 1 reported a decreased (THBϩ5␣THB)/THA ratio in GA treated rats, meaning that GA induces 11␤HSD2 activity rather than inhibits it. Because these measurements were incorrect, an experimental error can be assumed and therefore, the observed results are possibly also incorrect.…”

“…This is detected by an increased urinary ratio of active to inactive tetrahydro-(TH-) glucocorticoids. 3 In AME syndrome, the (THFϩ5␣THF)/THE ratios are increased to 20 to 50, as compared with normal values of 0.75 to 1.25. 3 Ruschitzka et al 1 reported a decreased (THBϩ5␣THB)/THA ratio in GA treated rats, meaning that GA induces 11␤HSD2 activity rather than inhibits it.…”