ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014
Feedforward activation of endothelial ENaC by high sodium.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 48 citations in OpenAlex.
- TET2 and CSMD1 genes affect SBP response to hydrochlorothiazide in never-treated essential hypertensives.Journal of hypertension · 2015Trial
- Time course and contributors to greater glycocalyx thickness and integrity following Western diet consumption.American journal of physiology. Heart and circulatory physiology · 2025Article
- SECS, drugs, and Rac1&Rho: regulation of EnNaC in vascular endothelial cells.Pflugers Archiv : European journal of physiology · 2025Article
- Activity and function of the endothelial sodium channel is regulated by the effector domain of MARCKS-like protein 1 in mouse aortic endothelial cells.American journal of physiology. Cell physiology · 2025Article
- Predictive value of estimated pulse wave velocity for cardiovascular and all-cause mortality in individuals with obesity.Diabetology & metabolic syndrome · 2023Article
- Advances in the Physiology of Transvascular Exchange and A New Look At Rational Fluid Prescription.International journal of general medicine · 2023Review
- Endothelial sodium channel activation mediates DOCA-salt-induced endothelial cell and arterial stiffening.Metabolism: clinical and experimental · 2022Article
- Rapid shear stress-dependent ENaC membrane insertion is mediated by the endothelial glycocalyx and the mineralocorticoid receptor.Cellular and molecular life sciences : CMLS · 2022Article
- Effects of amiloride on acetylcholine-dependent arterial vasodilation evolve over time in mice on a high salt diet.Physiological reports · 2022Article
- Role of the vascular endothelial sodium channel activation in the genesis of pathologically increased cardiovascular stiffness.Cardiovascular research · 2022Review
- High salt diet-induced proximal tubular phenotypic changes and sodium-glucose cotransporter-2 expression are coordinated by cold shock Y-box binding protein-1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Increased endothelial sodium channel activity by extracellular vesicles in human aortic endothelial cells: putative role of MLP1 and bioactive lipids.American journal of physiology. Cell physiology · 2021Article
- Epithelial Sodium Channel and Salt-Sensitive Hypertension.Hypertension (Dallas, Tex. : 1979) · 2021Review
- Endothelial Nanomechanics in the Context of Endothelial (Dys)function and Inflammation.Antioxidants & redox signaling · 2019Review
- Oxidized low-density lipoprotein stimulates epithelial sodium channels in endothelial cells of mouse thoracic aorta.British journal of pharmacology · 2018Article
- Salt-induced NaPflugers Archiv : European journal of physiology · 2017Article
- Involvement Of Vascular Aldosterone Synthase In Phosphate-Induced Osteogenic Transformation Of Vascular Smooth Muscle Cells.Scientific reports · 2017Article
- Nanomechanics of the endothelial glycocalyx contribute to NaScientific reports · 2017Article
- The Role of Uric Acid in Hypertension of Adolescents, Prehypertension and Salt Sensitivity of Blood Pressure.Medical science monitor : international medical journal of experimental and clinical research · 2017Review
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Corrections and comments
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kidney epithelial sodium channels (ENaCs) are known to be inactivated by high sodium concentrations (feedback inhibition). Recently, the endothelial sodium channel (EnNaC) was identified to control the nanomechanical properties of the endothelium. EnNaC-dependent endothelial stiffening reduces the release of nitric oxide, the hallmark of endothelial dysfunction. To study the regulatory impact of sodium on EnNaC, endothelial cells (EA.hy926 and ex vivo mouse endothelium) were incubated in aldosterone-free solutions containing either low (130 mM) or high (150 mM) sodium concentrations. By applying atomic force microscopy-based nanoindentation, an unexpected positive correlation between increasing sodium concentrations and cortical endothelial stiffness was observed, which can be attributed to functional EnNaC. In particular, an acute rise in sodium concentration (+20 mM) was sufficient to increase EnNaC membrane abundance by 90% and stiffening of the endothelial cortex by 18%. Despite the absence of exogenous aldosterone, these effects were prevented by the aldosterone synthase inhibitor FAD286 (100 nM) or the mineralocorticoid receptor (MR)-antagonist spironolactone (100 nM), indicating endogenous aldosterone synthesis and MR-dependent signaling. Interestingly, in the presence of high-sodium concentrations, FAD286 increased the transcription of the MR by 69%. Taken together, a novel feedforward activation of EnNaC by sodium is proposed that contrasts ENaC feedback inhibition in kidney.
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