ReviewActa pharmacologica Sinica2011
Role of the epithelial sodium channel in salt-sensitive hypertension.
Review in Acta pharmacologica Sinica, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 41 citations in OpenAlex.
- Differential Assembly of Native Epithelial Sodium Channel Complexes Across Mouse Epithelial Tissues.Kidney360 · 2026Article
- Differential Assembly of Native ENaC Complexes Across Mouse Epithelial Tissues.bioRxiv : the preprint server for biology · 2026Article
- The Effect of Renal Ischemia/Reperfusion on the Renal Expression of Epithelial Sodium Channels in Rat: Possible Role of Neural Precursor Cell-Expressed Developmentally Down-Regulated Protein (Nedd4-2).Kidney & blood pressure research · 2026Article
- Integrated mechanisms linking sodium-potassium imbalance to salt-sensitive hypertension.Physiological reports · 2025Review
- The Human Gut and Dietary Salt: TheNutrients · 2024Article
- The Role of Sodium-Glucose Cotransporter-2 Inhibitors in the Treatment Paradigm of CKD in Africa: An African Association of Nephrology Panel Position Paper.Kidney international reports · 2024Article
- Effects of a high-salt diet on MAP and expression levels of renal ENaCs and aquaporins in SHR.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- The role of dietary salt in metabolism and energy balance: Insights beyond cardiovascular disease.Diabetes, obesity & metabolism · 2023Review
- The optimization of electrochemical immunosensors to detect epithelial sodium channel as a biomarker of hypertension.ADMET & DMPK · 2023Article
- Role of Ion Channel Remodeling in Endothelial Dysfunction Induced by Pulmonary Arterial Hypertension.Biomolecules · 2022Review
- Epac1-/- and Epac2-/- mice exhibit deficient epithelial Na+ channel regulation and impaired urinary Na+ conservation.JCI insight · 2022Article
- Pathophysiology and genetics of salt-sensitive hypertension.Frontiers in physiology · 2022Review
- Article
- Mal protein stabilizes luminal membrane PLC-β3 and negatively regulates ENaC in mouse cortical collecting duct cells.American journal of physiology. Renal physiology · 2019Article
- Article
- Ion Channels in Pulmonary Hypertension: A Therapeutic Interest?International journal of molecular sciences · 2018Review
- Hypothalamic Ion Channels in Hypertension.Current hypertension reports · 2018Review
- Involvement of ENaC in the development of salt-sensitive hypertension.American journal of physiology. Renal physiology · 2017Review
- Oxidative Stress and Hypertensive Diseases.The Medical clinics of North America · 2017Review
- Norepinephrine-evoked salt-sensitive hypertension requires impaired renal sodium chloride cotransporter activity in Sprague-Dawley rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epithelial sodium channel (ENaC) is a heteromeric channel composed of three similar but distinct subunits, α, β and γ. This channel is an end-effector in the rennin-angiotensin-aldosterone system and resides in the apical plasma membrane of the renal cortical collecting ducts, where reabsorption of Na(+) through ENaC is the final renal adjustment step for Na(+) balance. Because of its regulation and function, the ENaC plays a critical role in modulating the homeostasis of Na(+) and thus chronic blood pressure. The development of most forms of hypertension requires an increase in Na(+) and water retention. The role of ENaC in developing high blood pressure is exemplified in the gain-of-function mutations in ENaC that cause Liddle's syndrome, a severe but rare form of inheritable hypertension. The evidence obtained from studies using animal models and in human patients indicates that improper Na(+) retention by the kidney elevates blood pressure and induces salt-sensitive hypertension.
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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.