Renin-Dependency of Glycyrrhizin-Induced Pseudoaldosteronism.

Kageyama, Yoichi; Suzuki, Hiromichi; Saruta, Takao

doi:10.1507/endocrj1954.38.103

Cited by 14 publications

(8 citation statements)

References 16 publications

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“…Review of that work suggests that a second perturbation of BP homoeostasis may be necessary for a hypertensive effect of 11β-HSD inhibition. For example, in a cohort treated with glycyrrhizin for 4 weeks, only those with plasma renin activity above 1.5 ng · ml −1 · h −1 had increases in their BP [23]. Mean plasma renin activity in our present cohort was 0.73 + − 0.59 ng · ml −1 · h −1 , below that threshold.…”

Section: Ga 11β-hsd Inhibition and Bpcontrasting

confidence: 49%

Glycyrrhetinic acid attenuates vascular smooth muscle vasodilatory function in healthy humans

et al. 2010

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Abnormal glucocorticoid metabolism contributes to vascular dysfunction and cardiovascular disease. Cortisol activation of vascular mineralocorticoid and glucocorticoid receptors is regulated by two types of 11beta-HSD (11-beta hydroxysteroid dehydrogenase), namely 11beta-HSD2 and 11beta-HSD1 (type 2 and type 1 11beta-HSD respectively). We hypothesized that inhibition of 11beta-HSD would attenuate vascular function in healthy humans. A total of 15 healthy subjects were treated with the selective 11beta-HSD inhibitor GA (glycyrrhetinic acid) or matching placebo in a randomized double-blinded cross-over trial. 11beta-HSD activity was assessed by the urinary cortisol/cortisone ratio, and vascular function was measured using strain-gauge plethysmography. Endothelial function was measured through incremental brachial artery administration of methacholine (0.3-10 microg/min) and vascular smooth muscle function with incremental verapamil (10-300 microg/min). GA increased the 24-h urinary cortisol/cortisone ratio compared with placebo (P=0.008). GA tended to reduce the FBF (forearm blood flow) response to methacholine (P=0.09) and significantly reduced the FBF response to verapamil compared with placebo (P=0.04). MAP (mean arterial pressure) did not differ between the study conditions. 11beta-HSD inhibition attenuated vascular smooth muscle vasodilatory function in healthy humans. Disturbances in cortisol activity resulting from 11beta-HSD inactivation is therefore a second plausible mechanism for mineralocorticoid-mediated hypertension in humans.

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Section: Ga 11β-hsd Inhibition and Bpcontrasting

confidence: 49%

Glycyrrhetinic acid attenuates vascular smooth muscle vasodilatory function in healthy humans

et al. 2010

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“…The incidence is dose‐dependent and differs among subjects: side‐effects occur more often in conditions favouring sodium retention, such as pre‐menstrual period or oral contraceptive use, and are facilitated by subclinical diseases as borderline hypertension and high plasma renin activity 20 , . 21 …”

Section: Side‐effectsmentioning

confidence: 99%

glycyrrhizin as a potential treatment for chronic hepatitis C

Rossum

Vulto

Man

et al. 1998

Aliment Pharmacol Ther

249

147

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Chronic hepatitis C is a slowly progressive liver disease that may evolve into cirrhosis with its potential complications of liver failure or hepatocellular carcinoma. Current therapy with α‐interferon is directed at viral clearance, but sustained response is only achieved in 20–40% of patients without cirrhosis, and less than 20% in patients with cirrhosis who have the greatest need for therapy. Treatment for those who do not respond to anti‐viral therapy is highly desirable. In Japan glycyrrhizin has been used for more than 20 years as treatment for chronic hepatitis. In randomized controlled trials, glycyrrhizin induced a significant reduction of serum aminotransferases and an improvement in liver histology compared to placebo. Recently, these short‐term effects have been amplified by a well‐conducted retrospective study suggesting that long‐term usage of glycyrrhizin prevents development of hepatocellular carcinoma in chronic hepatitis C. The mechanism by which glycyrrhizin improves liver biochemistry and histology are undefined. Metabolism, pharmacokinetics, side‐effects, and anti‐viral and hepatoprotective effects of glycyrrhizin are discussed.

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“…1). There were evidence from numerous clinical case reports and trials that conventional administration of GL may cause pseudohypercorticosteroidism, such as sodium and water retention, hypertension and hypokalaemia (Van Rossum et al, 2001;Kageyama et al, 1991;Shintani et al, 1992). Generally, the mechanism of this side effect was induced by GA competitive inhibition of hepatic microsomal 11B-typeII hydroxysteroid dehydrogenase (11-HSD2) activity, which indirectly enhance cortical hormone concentration, showing the effect of steroids (Kratschmar et al, 2011).…”

Section: Introductionmentioning

confidence: 99%