The endothelial ?ENaC contributes to vascular endothelial function in vivo.

ABSTRACT: The Epithelial Sodium Channel (ENaC) is a key player in renal sodium homeostasis. The expression of ? ? ? ENaC subunits has also been described in the endothelium and vascular smooth muscle, suggesting a role in vascular function. We recently demonstrated that endothelial ENaC is involved in aldosterone-modulated endothelial stiffness. Here we explore the functional role of the endothelial ?ENaC subunit in vascular function in vivo. Compared to littermates, mice with conditional ?ENaC subunit gene inactivation in the endothelium only (endo-?ENaC 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 ?ENaC 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-?ENaC KO mice, suggesting a critical role of endothelial ENaC in agonist-induced nitric oxide production. In endo-?ENaC KO mice, compensatory mechanisms occurred and steady state vascular function was not altered except for flow-mediated dilation. Our data suggest that endothelial ?ENaC contributes to vascular endothelial function in vivo.

SUBMITTER: Tarjus A 

PROVIDER: S-EPMC5614594 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature