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In the absence of aldosterone, a rise in extracellular sodium (&gt;145 mM) increases EnNaC surface abundance, thereby stiffening the cortex of vascular endothelial cells (ECs)\n                    <jats:italic>in vitro.<\/jats:italic>\n                    The latter reduces the release of NO\u2014the hallmark of endothelial dysfunction. Here, we test whether high extracellular sodium\n                    <jats:italic>per se<\/jats:italic>\n                    increases EnNaC expression and cortical stiffness in an aldosterone synthase (\n                    <jats:italic>Cyp11b2<\/jats:italic>\n                    )\n                    <jats:italic>\u2010<\/jats:italic>\n                    deficient (AS\n                    <jats:sup>\u2010\/\u2010<\/jats:sup>\n                    ) mouse model. Therefore, we employed\n                    <jats:italic>in situ<\/jats:italic>\n                    ECs of\n                    <jats:italic>ex vivo<\/jats:italic>\n                    aorta preparations from wild\u2010type (WT) and AS\n                    <jats:sup>\u2010\/\u2010<\/jats:sup>\n                    . EnNaC surface expression (\u201016%) and cortical stiffness (\u201022%) were reduced in AS\n                    <jats:sup>\u2010\/\u2010<\/jats:sup>\n                    , compared with WT, whereas NO secretion was exclusively detectable in AS\n                    <jats:sup>\u2010\/\u2010<\/jats:sup>\n                    . EnNaC inhibition with benzamil decreased stiffness in both, while mineralocorticoid receptor antagonism diminished stiffness only in the WT. In the absence of aldosterone, high sodium (150 mM) increased EnNaC surface expression\n                    <jats:italic>ex vivo<\/jats:italic>\n                    (plus 19%) and cortical stiffness\n                    <jats:italic>ex vivo<\/jats:italic>\n                    (plus 41%) and\n                    <jats:italic>in vivo<\/jats:italic>\n                    (plus 44%). Application of aldosterone adjusted the stiffness of AS\n                    <jats:sup>\u2010\/\u2010<\/jats:sup>\n                    to the WT level. We conclude that high sodium\n                    <jats:italic>per se<\/jats:italic>\n                    determines EnNaC expression and consequently endothelial cortical nanomechanics, thus likely contributing to endothelial dysfunction.\u2014Jeggle, P., Hofschr\u00f6er, V., Maase, M., Bertog, M., Kusche\u2010Vihrog, K. Aldosterone synthase knockout mouse as a model for sodium\u2010induced endothelial sodium channel up\u2010regulation in vascular endothelium.\n                    <jats:italic>FASEB J.<\/jats:italic>\n                    30, 45\u201053 (2016).\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.14-259606","type":"journal-article","created":{"date-parts":[[2015,8,31]],"date-time":"2015-08-31T22:29:08Z","timestamp":1441060148000},"page":"45-53","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Aldosterone synthase knockout mouse as a model for sodium\u2010induced endothelial sodium channel up\u2010regulation in vascular endothelium"],"prefix":"10.1096","volume":"30","author":[{"given":"Pia","family":"Jeggle","sequence":"first","affiliation":[{"name":"Institute of Physiology II, University of Munster Munster Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Verena","family":"Hofschr\u00f6er","sequence":"additional","affiliation":[{"name":"Institute of Physiology II, University of Munster Munster Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martina","family":"Maase","sequence":"additional","affiliation":[{"name":"Institute of Physiology II, University of Munster Munster Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marko","family":"Bertog","sequence":"additional","affiliation":[{"name":"Institut f\u00fcr Zellul\u00e4re und Molekulare Physiologie, Friedrich\u2010Alexander Universit\u00e4t Erlangen\u2010N\u00fcrnberg Erlangen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kristina","family":"Kusche\u2010Vihrog","sequence":"additional","affiliation":[{"name":"Institute of Physiology II, University of Munster Munster Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2015,8,31]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1161\/CIR.0b013e3182009701"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005050460"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00973.x"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/0039-128X(94)00026-9"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2005-0681"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1995.269.4.E657"},{"key":"e_1_2_7_8_1","doi-asserted-by":"crossref","first-page":"425","DOI":"10.1042\/cs1030425","article-title":"Aldosterone induces acute endothelial dysfunction in vivo in humans: evidence for an aldosterone\u2010induced vasculopathy","volume":"103","author":"Farquharson C. 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