Pseudohyperaldosteronism: Pathogenetic Mechanisms

Armanini, Decio; Calò, Lorenzo A.; Semplicini, Andrea

doi:10.1080/713609355

Cited by 30 publications

(22 citation statements)

References 135 publications

(265 reference statements)

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“…Liqourice-induced hypertension with hypokalemia must be differentiated from other genetic deficiencies which may present with similar findings: three monogenetic types of mineralo-corticoid hypertension have been identified, Liddle's syndrome, glucocorticoid-remediable hypertension, and apparent mineralo-corticoid excess, an autosomal recessive disorder with mutations in the 11β-HSD2 gene [36][37][38][39]. Use of chewing and sucking tobacco snuffs and other products containing liquorice-like herbal medications, teas, breath fresheners, chewing gums, alcoholic drinks, and food products, all contribute to chronic habitual frequent swallowing of large quantities of liquorice [34,35].…”

Section: Discussionmentioning

confidence: 99%

Liquorice Health Check, Oro-Dental Implications, and a Case Report

Touyz

2009

Case Reports in Medicine

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Liquorice has an active substance, Glycyrrhizin which inhibits the conversion of precursor cortisol to cortisone by inhibiting the enzyme 11-betahydroxysteroid dehydrogenase. When imbibed, liquorice acts like hyperaldosteronism which presents with typical symptoms including high blood pressure, low blood potassium, and muscle pain and weakness. This article appraises physiological and pharmacological effects on health of liquorice, critiques products containing liquorice, describes a typical case report of liquorice-induced hypertension, and appraises oral effects from consumption of liquorice products.

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Section: Discussionmentioning

confidence: 99%

Liquorice Health Check, Oro-Dental Implications, and a Case Report

Touyz

2009

Case Reports in Medicine

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“…Although CBX has been described to be devoid of effects on neuronal excitability (Köhling et al. 2001), it affects several ionic channels and receptors (Armanini et al. 2003; Salvi et al.…”

Section: Discussionmentioning

confidence: 99%

“…Although CBX has been described to be devoid of effects on neuronal excitability (Köhling et al 2001), it affects several ionic channels and receptors (Armanini et al 2003;Salvi et al 2005). Furthermore, the CBX-induced suppression of spontaneous synchronous activity in neurons was still present in connexin-43 knock-out mice (Rouach et al 2003).…”

Section: Discussionmentioning

confidence: 99%

Gap‐junction blocker carbenoxolone differentially enhances NMDA‐induced cell death in hippocampal neurons and astrocytes in co‐culture

Zündorf

Kahlert

Reiser

2007

Journal of Neurochemistry

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The beneficial or detrimental role of gap junction communication in the pathophysiology of brain injury is still controversial. We used co-cultures of hippocampal astrocytes and neurons, where we identified homocellular astrocyte-astrocyte and heterocellular astrocyte-neuron coupling by fluorescence recovery after photobleaching, which was decreased by the gap junction blocker carbenoxolone (CBX). In these cultures, we determined the cell type-specific effects of CBX on the excitotoxic damage caused by N-methyl-D-aspartate (NMDA). We determined in both astrocytes and neurons the influence of CBX, alone or together with NMDA challenge, on cytotoxicity using propidium iodide labeling. CBX alone was not cytotoxic, but CBX treatment differentially accelerated the NMDA-induced cell death in both astrocytes and neurons. In addition, we measured mitochondrial potential using rhodamine 123, membrane potential using the oxonol dye bis(1,3-diethylthiobarbituric acid)trimethine oxonol, cytosolic Ca 2+ level using fura-2, and formation of reactive oxygen species (ROS) using dihydroethidium. CBX alone induced neither an intracellular Ca 2+ rise nor a membrane depolarization. However, CBX elicited a mitochondrial depolarization in both astrocytes and neurons and increased the ROS formation in neurons. In contrast, NMDA caused a membrane depolarization in neurons, coinciding with intracellular Ca 2+ rise, but neither mitochondrial depolarization nor ROS production seem to be involved in NMDA-mediated cytotoxicity. Pretreatment with CBX accelerated the NMDA-induced membrane depolarization and prevented the repolarization of neurons after the NMDA challenge. We hypothesize that these effects are possibly mediated via blockage of gap junctions, and might be involved in the mechanism of CBXinduced acceleration of excitotoxic cell death, whereas the CBX-induced mitochondrial depolarization and ROS formation are not responsible for the increase in cytotoxicity. We conclude that both in astrocytes and neurons gap junctions provide protection against NMDA-induced cytotoxicity.

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“…With prolonged treatment, Cbx produces a pseudohyperaldosteronism by binding to mineralocorticoid receptors and inhibiting 11␤-hydroxysteroid dehydrogenase (11HSD) type 2 at the level of epithelial target tissues for aldosterone (2). Cbx also has central hypertensive effects, without affecting saline appetite, when injected into a lateral ventricle (3).…”

mentioning

confidence: 99%

Carbenoxolone Induces Oxidative Stress in Liver Mitochondria, Which Is Responsible for Transition Pore Opening

et al. 2005

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Carbenoxolone (Cbx), a derivative of glycyrrhetinic acid, which has been found to affect mineralocorticoid and glucocorticoid receptors, induces swelling and membrane potential collapse when added to Ca(2+)-loaded liver mitochondria at 10 microM concentrations. These effects are strictly correlated with hydrogen peroxide generation, increase in oxygen uptake, and sulfhydryl and pyridine nucleotide oxidation. Cyclosporin A, bongkrekic acid, and N-ethylmaleimide completely abolish all the above-described effects, suggesting that Cbx can be considered an inducer of mitochondrial permeability transition by means of oxidative stress. Cbx can also trigger the apoptotic pathway because the above events are also correlated with the loss of cytochrome c. These effects are probably related to the conjugated carbonyl oxygen in C-11, which produces reactive oxygen species by interacting with the mitochondrial respiratory chain, mainly at the level of complex I but, most likely, also with complex III. The oxidative stress induced by Cbx, which is responsible for pore opening, excludes that this is related to a genomic effect of the compound.

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Pseudohyperaldosteronism: Pathogenetic Mechanisms

Cited by 30 publications

References 135 publications

Liquorice Health Check, Oro-Dental Implications, and a Case Report

Liquorice Health Check, Oro-Dental Implications, and a Case Report

Gap‐junction blocker carbenoxolone differentially enhances NMDA‐induced cell death in hippocampal neurons and astrocytes in co‐culture

Carbenoxolone Induces Oxidative Stress in Liver Mitochondria, Which Is Responsible for Transition Pore Opening

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