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However, the role of endothelial ENaCs<\/jats:styled-content> in salt\u2010sensitive hypertension remains unclear. Here, we have investigated how endothelial ENaCs<\/jats:styled-content> in Sprague\u2010Dawley (SD<\/jats:styled-content>) rats respond to high\u2010salt (HS<\/jats:styled-content>) challenge.<\/jats:p><\/jats:sec>Experimental Approach<\/jats:title>BP<\/jats:styled-content> and plasma aldosterone levels were measured. We used patch\u2010clamp technique to record ENaC<\/jats:styled-content> activity in split\u2010open mesenteric arteries (MAs<\/jats:styled-content>). Western blot and G<\/jats:styled-content>riess assay were used to detect expression of \u03b1\u2010ENaCs<\/jats:styled-content>, eNOS and NO<\/jats:styled-content>. Vasorelaxation in second\u2010order MAs<\/jats:styled-content> was measured with wire myograph assays.<\/jats:p><\/jats:sec>Key Results<\/jats:title>Functional ENaCs<\/jats:styled-content> were observed in endothelial cells and their activity was significantly decreased after 1 week of HS<\/jats:styled-content> diet. After 3 weeks of HS<\/jats:styled-content> diet, ENaC<\/jats:styled-content> expression was also reduced. When either ENaC<\/jats:styled-content> activity or expression was reduced, endothelium\u2010dependent relaxation (EDR<\/jats:styled-content>) of MAs<\/jats:styled-content>, in response to ACh<\/jats:styled-content>, was enhanced. This enhancement of EDR<\/jats:styled-content> was mimicked by amiloride, a blocker of ENaCs<\/jats:styled-content>. By contrast, HS<\/jats:styled-content> diet significantly increased contractility of MAs<\/jats:styled-content>, accompanied by decreased eNOS<\/jats:styled-content> activity and NO<\/jats:styled-content> levels. However, ACh<\/jats:styled-content>\u2010induced release of NO<\/jats:styled-content> was much higher in MAs<\/jats:styled-content> isolated from HS<\/jats:styled-content> rats than those from NS<\/jats:styled-content> rats.<\/jats:p><\/jats:sec>Conclusions and Implications<\/jats:title>HS<\/jats:styled-content> intake increased the BP<\/jats:styled-content> of SD<\/jats:styled-content> rats, but simultaneously enhanced EDR<\/jats:styled-content> by reducing ENaC<\/jats:styled-content> activity and expression due to feedback inhibition. Therefore, ENaCs<\/jats:styled-content> may play an important role in endothelial cells allowing the vasculature to adapt to HS<\/jats:styled-content> conditions.<\/jats:p><\/jats:sec>Linked Articles<\/jats:title>This article is part of a themed section on Chinese Innovation in Cardiovascular Drug Discovery. To view the other articles in this section visit http:\/\/dx.doi.org\/10.1111\/bph.2015.172.issue-23<\/jats:ext-link><\/jats:p><\/jats:sec>","DOI":"10.1111\/bph.13185","type":"journal-article","created":{"date-parts":[[2015,5,8]],"date-time":"2015-05-08T06:13:11Z","timestamp":1431065591000},"page":"5634-5646","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":37,"title":["Dietary salt regulates epithelial sodium channels in rat endothelial cells: adaptation of vasculature to salt"],"prefix":"10.1111","volume":"172","author":[{"given":"Hui\u2010Bin","family":"Liu","sequence":"first","affiliation":[{"name":"Departments of Clinical Pharmacy and Cardiology Institute of Clinical Pharmacy, the 2nd Affiliated Hospital, Harbin Medical University, Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment Harbin 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