ArticleBritish journal of pharmacology2015
Dietary salt regulates epithelial sodium channels in rat endothelial cells: adaptation of vasculature to salt.
Article in British journal of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- KAT7 contributes to ponatinib-induced hypertension by promoting endothelial senescence and inflammatory responses through activating NF-κB signaling pathway.Journal of hypertension · 2025Article
- Fusaric acid-mediated S-glutathionylation of MaAKT1 channel confers the virulence of Foc TR4 to banana.PLoS pathogens · 2025Article
- Perinatal Exposure of Dams to a High Salt Diet Impaired Vascular Function and Elevated Biomarkers of Inflammation in the Offspring.Clinical Medicine Insights. Cardiology · 2025Article
- 2-(4-Methylthiazol-5-yl) Ethyl Nitrate Hydrochloride Ameliorates Cognitive Impairment via Modulation of Oxidative Stress and Nuclear Factor Kappa B (NF-κB) Signaling Pathway in Chronic Cerebral Hypoperfusion-Associated Spontaneously Hypertensive Rats.Antioxidants (Basel, Switzerland) · 2024Article
- Epithelial NaComprehensive Physiology · 2024Review
- Clinical and cardiac characteristics of primary bilateral macronodular adrenal hyperplasia.Journal of medical biochemistry · 2024Article
- The co-expression of the depolarizing and hyperpolarizing mechanosensitive ion channels in mammalian retinal neurons.Frontiers in medicine · 2024Article
- Endothelial sodium channel activation mediates DOCA-salt-induced endothelial cell and arterial stiffening.Metabolism: clinical and experimental · 2022Article
- Effects of amiloride on acetylcholine-dependent arterial vasodilation evolve over time in mice on a high salt diet.Physiological reports · 2022Article
- Aldosterone-stimulated endothelial epithelial sodium channel (EnNaC) plays a role in cold exposure-induced hypertension in rats.Frontiers in pharmacology · 2022Article
- Salt Sensitivity of Blood Pressure in Blacks and Women: A Role of Inflammation, Oxidative Stress, and Epithelial NaAntioxidants & redox signaling · 2021Review
- Immune Mechanisms of Dietary Salt-Induced Hypertension and Kidney Disease: Harry Goldblatt Award for Early Career Investigators 2020.Hypertension (Dallas, Tex. : 1979) · 2021Review
- Epithelial Sodium Channel and Salt-Sensitive Hypertension.Hypertension (Dallas, Tex. : 1979) · 2021Review
- Homocysteine Causes Endothelial Dysfunction via Inflammatory Factor-Mediated Activation of Epithelial Sodium Channel (ENaC).Frontiers in cell and developmental biology · 2021Article
- Insulin Resistance and Pellino-1 Mediated Decrease in the Activities of Vasodilator Signaling Contributes to Sunitinib-Induced Hypertension.Frontiers in pharmacology · 2021Article
- Sodium-not harmful?Pediatric nephrology (Berlin, Germany) · 2020Article
- High salt-induced weakness of anti-oxidative function of natriuretic peptide receptor-C and podocyte damage in the kidneys of Dahl rats.Chinese medical journal · 2020Article
- Stimulation of Epithelial Sodium Channels in Endothelial Cells by Bone Morphogenetic Protein-4 Contributes to Salt-Sensitive Hypertension in Rats.Oxidative medicine and cellular longevity · 2020Article
- The Absence of Endothelial Sodium Channel α (αENaC) Reduces Renal Ischemia/Reperfusion Injury.International journal of molecular sciences · 2019Article
- New insights regarding epithelial Na+ channel regulation and its role in the kidney, immune system and vasculature.Current opinion in nephrology and hypertension · 2019Review
Corrections and comments
- Erratum issuedErratum.2017
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
background and purposeThe epithelial sodium channel (ENaC) is expressed in vascular endothelial cells and is a negative modulator of vasodilation. However, the role of endothelial ENaCs in salt-sensitive hypertension remains unclear. Here, we have investigated how endothelial ENaCs in Sprague-Dawley (SD) rats respond to high-salt (HS) challenge. EXPERIMENTAL APPROACH: BP and plasma aldosterone levels were measured. We used patch-clamp technique to record ENaC activity in split-open mesenteric arteries (MAs). Western blot and Griess assay were used to detect expression of α-ENaCs, eNOS and NO. Vasorelaxation in second-order MAs was measured with wire myograph assays. KEY
resultsFunctional ENaCs were observed in endothelial cells and their activity was significantly decreased after 1 week of HS diet. After 3 weeks of HS diet, ENaC expression was also reduced. When either ENaC activity or expression was reduced, endothelium-dependent relaxation (EDR) of MAs, in response to ACh, was enhanced. This enhancement of EDR was mimicked by amiloride, a blocker of ENaCs. By contrast, HS diet significantly increased contractility of MAs, accompanied by decreased eNOS activity and NO levels. However, ACh-induced release of NO was much higher in MAs isolated from HS rats than those from NS rats. CONCLUSIONS AND IMPLICATIONS: HS intake increased the BP of SD rats, but simultaneously enhanced EDR by reducing ENaC activity and expression due to feedback inhibition. Therefore, ENaCs may play an important role in endothelial cells allowing the vasculature to adapt to HS conditions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.