ArticleBritish journal of pharmacology2018
Dietary salt blunts vasodilation by stimulating epithelial sodium channels in endothelial cells from salt-sensitive Dahl rats.
Article in British journal of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- Role of skeletal muscle perfusion and insulin resistance in the effect of dietary sodium on heart function in overweight.ESC heart failure · 2021Trial
- Epithelial sodium channel in dendritic cells participates in high-fat-induced inflammatory responses.Molecular biology reports · 2025Article
- Endothelial MicroRNA-214 Confers Angiotensin II Hypertension by Targeting eNOS in Mice.Kidney & blood pressure research · 2025Article
- Hypertension toxicity of VEGFR-TKIs in cancer treatment: incidence, mechanisms, and management strategies.Archives of toxicology · 2025Review
- 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
- Association Between ABCA1 Gene Polymorphisms and the Risk of Hypertension in the Chinese Han Population.Frontiers in public health · 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
- Insulin Resistance and Pellino-1 Mediated Decrease in the Activities of Vasodilator Signaling Contributes to Sunitinib-Induced Hypertension.Frontiers in pharmacology · 2021Article
- Homocysteine Causes Endothelial Dysfunction via Inflammatory Factor-Mediated Activation of Epithelial Sodium Channel (ENaC).Frontiers in cell and developmental biology · 2021Article
- 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
- Lovastatin attenuates hypertension induced by renal tubule-specific knockout of ATP-binding cassette transporter A1, by inhibiting epithelial sodium channels.British journal of pharmacology · 2019Article
- 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
- Epithelial Sodium Channel in Aldosterone-Induced Endothelium Stiffness and Aortic Dysfunction.Hypertension (Dallas, Tex. : 1979) · 2018Article
- Dietary salt blunts vasodilation by stimulating epithelial sodium channels in endothelial cells from salt-sensitive Dahl rats.British journal of pharmacology · 2018Article
- Spotlight on small molecules in cardiovascular diseases.British journal of pharmacology · 2018Article
- Oxidized low-density lipoprotein stimulates epithelial sodium channels in endothelial cells of mouse thoracic aorta.British journal of pharmacology · 2018Article
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
background and purposeOur recent studies show that the reduced activity of epithelial sodium channels (ENaC) in endothelial cells accounts for the adaptation of vasculature to salt in Sprague-Dawley rats. The present study examines a hypothesis that enhanced ENaC activity mediates the loss of vasorelaxation in Dahl salt-sensitive (SS) rats. EXPERIMENTAL APPROACH: We used the cell-attached patch-clamp technique to record ENaC activity in split-open mesenteric arteries. Western blot and immunofluorescence staining were used to evaluate the levels of aldosterone, ENaC, eNOS and NO. Blood pressure was measured with the tail-cuff method and the artery relaxation was measured with the wire myograph assay. KEY
resultsHigh-salt (HS) diet significantly increased plasma aldosterone and ENaC activity in the endothelial cells of Dahl SS rats. The endothelium-dependent artery relaxation was blunted by HS challenge in these rats. Amiloride, a potent blocker of ENaC, increased both phosphorylated eNOS and NO and therefore prevented the HS-induced loss of vasorelaxation. As, in SS rats, endogenous aldosterone was already elevated by HS challenge, exogenous aldosterone did not further elevate ENaC activity in the rats fed with HS. Eplerenone, a mineralocorticoid receptor antagonist, attenuated the effects of HS on both ENaC activity and artery relaxation. CONCLUSIONS AND IMPLICATIONS: These data suggest that HS diet blunts artery relaxation and causes hypertension via a pathway associated with aldosterone-dependent activation of ENaC in endothelial cells. This pathway provides one of the mechanisms by which HS causes hypertension in Dahl SS rats. LINKED ARTICLES: This article is part of a themed section on Spotlight on Small Molecules in Cardiovascular Diseases. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.8/issuetoc.
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