The endothelial αENaC contributes to vascular endothelial function in vivo

Abstract : The Epithelial Sodium Channel (ENaC) is a key player in renal sodium homeostasis. The expression of α β γ ENaC subunits has also been described in the endothelium and vascular smooth muscle, suggesting a role in vascular function. We recently demonstrated that endo-thelial ENaC is involved in aldosterone-modulated endothelial stiffness. Here we explore the functional role of the endothelial αENaC subunit in vascular function in vivo. Compared to lit-termates, mice with conditional αENaC subunit gene inactivation in the endothelium only (endo-αENaC Knock Out mice) had no difference in their physiological parameters such as systolic blood pressure or heart rate. Acute and long-term renal Na + handlings were not affected, indicating that endothelial αENaC subunit is not involved in renal sodium balance. Pharmacological inhibition of ENaC with benzamil blunted acetylcholine-induced nitric oxide production in mesenteric arteries from wild type mice but not in endo-αENaC KO mice, suggesting a critical role of endothelial ENaC in agonist-induced nitric oxide production. In endo-αENaC KO mice, compensatory mechanisms occurred and steady state vascular function was not altered except for flow-mediated dilation. Our data suggest that endothelial αENaC contributes to vascular endothelial function in vivo.
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PLoS ONE, Public Library of Science, 2017, 12 (9), pp.e0185319. 〈10.1371/journal.pone.0185319〉
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Antoine Tarjus, Martina Maase, Pia Jeggle, Ernesto Martinez-Martinez, Céline Fassot, et al.. The endothelial αENaC contributes to vascular endothelial function in vivo. PLoS ONE, Public Library of Science, 2017, 12 (9), pp.e0185319. 〈10.1371/journal.pone.0185319〉. 〈hal-01618147〉

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