Na+ homeostasis by epithelial Na+ channel (ENaC) and Nax channel (Nax): cooperation of ENaC and Nax

Marunaka, Yoshinori; Marunaka, Rie; Sun, Hai‐Ying; Yamamoto, Toshiro; Kanamura, Narisato; Taruno, Akiyuki

doi:10.21037/atm.2016.10.42

Cited by 12 publications

(18 citation statements)

References 65 publications

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“…Previously, low salt diet or application of aldosterone was observed to induce the expression of the αENaC subunit in the kidney, accompanied with unchanged expression for βand γENaC subunits [5,[92][93][94][95][96], which was also not observed in this study. Accordingly, compensatory effects for maintaining sodium homeostasis are realized via the colon and kidney rather than taste tissue with regard to adaptations in ENaC expression, indicating the pivotal role of these tissues in sodium reabsorption [97,98].…”

Section: Discussionmentioning

confidence: 99%

Sodium Imbalance in Mice Results Primarily in Compensatory Gene Regulatory Responses in Kidney and Colon, but Not in Taste Tissue

2020

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Renal excretion and sodium appetite provide the basis for sodium homeostasis. In both the kidney and tongue, the epithelial sodium channel (ENaC) is involved in sodium uptake and sensing. The diuretic drug amiloride is known to block ENaC, producing a mild natriuresis. However, amiloride is further reported to induce salt appetite in rodents after prolonged exposure as well as bitter taste impressions in humans. To examine how dietary sodium content and amiloride impact on sodium appetite, mice were subjected to dietary salt and amiloride intervention and subsequently analyzed for ENaC expression and taste reactivity. We observed substantial changes of ENaC expression in the colon and kidney confirming the role of these tissues for sodium homeostasis, whereas effects on lingual ENaC expression and taste preferences were negligible. In comparison, prolonged exposure to amiloride-containing drinking water affected β- and αENaC expression in fungiform and posterior taste papillae, respectively, next to changes in salt taste. However, amiloride did not only change salt taste sensation but also perception of sucrose, glutamate, and citric acid, which might be explained by the fact that amiloride itself activates bitter taste receptors in mice. Accordingly, exposure to amiloride generally affects taste impression and should be evaluated with care.

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Section: Discussionmentioning

confidence: 99%

Sodium Imbalance in Mice Results Primarily in Compensatory Gene Regulatory Responses in Kidney and Colon, but Not in Taste Tissue

2020

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“…Patients with Liddle’s syndrome, an autosomal dominant form of hereditary hypertension, carry gain-of-function mutations in ENaC genes, which disrupt ubiquitination sites of the channel. The deficiency of ubiquitination causes a constitutively increased number of ENaCs located in the apical membrane of the collecting duct epithelial cell of the kidney [ 67 , 68 , 69 , 70 , 71 , 72 , 73 , 74 , 75 , 76 ], leading to constitutively high ENaC-mediated renal Na + reabsorption and, thereby elevated body fluid volume. The phenomenon observed in Liddle’s syndrome strongly indicates that the expression of ENaCs plays an essential role in control of blood pressure.…”

Section: Roles Of Enac In Control Of Blood Pressurementioning

confidence: 99%

Actions of Quercetin, a Polyphenol, on Blood Pressure

et al. 2017

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Disorder of blood pressure control causes serious diseases in the cardiovascular system. This review focuses on the anti-hypertensive action of quercetin, a flavonoid, which is one of the polyphenols characterized as the compounds containing large multiples of phenol structural units, by varying the values of various blood pressure regulatory factors, such as vascular compliance, peripheral vascular resistance, and total blood volume via anti-inflammatory and anti-oxidant actions. In addition to the anti-inflammatory and anti-oxidant actions of quercetin, we especially describe a novel mechanism of quercetin’s action on the cytosolic Cl− concentration ([Cl−]c) and novel roles of the cytosolic Cl− i.e., (1) quercetin elevates [Cl−]c by activating Na+-K+-2Cl− cotransporter 1 (NKCC1) in renal epithelial cells contributing to Na+ reabsorption via the epithelial Na+ channel (ENaC); (2) the quercetin-induced elevation of [Cl−]c in renal epithelial cells diminishes expression of ENaC leading to a decrease in renal Na+ reabsorption; and (3) this reduction of ENaC-mediated Na+ reabsorption in renal epithelial cells drops volume-dependent elevated blood pressure. In this review, we introduce novel, unique mechanisms of quercetin’s anti-hypertensive action via activation of NKCC1 in detail.

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“…Membrane potential has been shown to be important for some virus entry, and in the case of human Rhinovirus Type 2 infection the membrane hyperpolarization enhances infection 30 . Inhibition of membrane depolarization is part of viral lung infection strategy, as shown for SARS-CoV 21 [34][35][36] . Following Na + influx via ENaC, the cells also present downstream mRNA synthesis elevation of inflammatory mediators 36 .…”

Section: Nacl Induces Cell Membrane Depolarization In a Dose-dependenmentioning

confidence: 99%

“…Inhibition of membrane depolarization is part of viral lung infection strategy, as shown for SARS-CoV 21 [34][35][36] . Following Na + influx via ENaC, the cells also present downstream mRNA synthesis elevation of inflammatory mediators 36 . In the same line, Na x expression blockade can improve scarring 36 .…”

Section: Nacl Induces Cell Membrane Depolarization In a Dose-dependenmentioning

confidence: 99%

“…Following Na + influx via ENaC, the cells also present downstream mRNA synthesis elevation of inflammatory mediators 36 . In the same line, Na x expression blockade can improve scarring 36 . Therefore, extracellular Na + imbalance through ENac inefficiency by SARS-CoV-2 infection may explain the formation of pulmonary fibrosis due to virus infection…”

Section: Nacl Induces Cell Membrane Depolarization In a Dose-dependenmentioning

confidence: 99%

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Hypertonic saline solution inhibits SARS-CoV-2 in vitro assay

Machado

Glaser

Araújo

et al. 2020

Preprint

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We are facing an unprecedented global health crisis caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). At this date more than 680 thousand people have died due to coronavirus disease 2019 (COVID-19). Unfortunately, until now no effective treatment to combat the virus and vaccine are available. We performed experiments to test if hypertonic saline solution is able to inhibit virus replication in vitro. Our data shows that 260 mM NaCl (1.5%) inhibits 100% SARS-CoV-2 replication in Vero cells. Furthermore, our results suggest that the virus replication inhibition is due to an intracellular mechanism and not due to the dissociation between spike SARS-CoV-2 protein and its human receptor angiotensin-converting enzyme 2 interaction. NaCl depolarizes the plasma membrane supposedly associated with the inhibition of the SARS-CoV-2 life cycle. This observation could lead to simple, safe and low cost interventions at various stages of COVID-19 treatment, improving the prognosis of infected patients, thereby mitigating the social and economic costs of the pandemic.

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Na+ homeostasis by epithelial Na+ channel (ENaC) and Nax channel (Nax): cooperation of ENaC and Nax

Cited by 12 publications

References 65 publications

Sodium Imbalance in Mice Results Primarily in Compensatory Gene Regulatory Responses in Kidney and Colon, but Not in Taste Tissue

Sodium Imbalance in Mice Results Primarily in Compensatory Gene Regulatory Responses in Kidney and Colon, but Not in Taste Tissue

Actions of Quercetin, a Polyphenol, on Blood Pressure

Hypertonic saline solution inhibits SARS-CoV-2 in vitro assay

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