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Recently, the endothelial sodium channel (EnNaC) was identified to control the nanomechanical properties of the endothelium. EnNaC\u2010dependent 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\n                    <jats:italic>ex vivo<\/jats:italic>\n                    mouse endothelium) were incubated in aldosterone\u2010free solutions containing either low (130 mM) or high (150 mM) sodium concentrations. By applying atomic force microscopy\u2010based 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)\u2010antagonist spironolactone (100 nM), indicating endogenous aldosterone synthesis and MR\u2010dependent signaling. Interestingly, in the presence of high\u2010sodium 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.\u2014Korte, S., Str\u00e4ter, A. S., Dr\u00fcppel, V., Oberleithner, H., Jeggle, P., Grossmann, C., Fobker, M., Nofer, J.\u2010R., Brand, E., Kusche\u2010Vihrog, K. Feedforward activation of endothelial ENaC by high sodium.\n                    <jats:italic>FASEB J.<\/jats:italic>\n                    28, 4015\u20104025 (2014).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.14-250282","type":"journal-article","created":{"date-parts":[[2014,5,28]],"date-time":"2014-05-28T01:31:55Z","timestamp":1401240715000},"page":"4015-4025","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":43,"title":["Feedforward activation of endothelial ENaC by high sodium"],"prefix":"10.1096","volume":"28","author":[{"given":"Stefanie","family":"Korte","sequence":"first","affiliation":[{"name":"Institute of Physiology II, University of M\u00fcnster M\u00fcnster Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexandra 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