ReviewThe Journal of biological chemistry2010
Epithelial Na+ channel (ENaC), hormones, and hypertension.
Review in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 95 citations in OpenAlex.
- Genetic variation in CYP4A11 and blood pressure response to mineralocorticoid receptor antagonism or ENaC inhibition: an exploratory pilot study in African Americans.Journal of the American Society of Hypertension : JASH · 2014Trial
- Epithelial sodium channel inhibition by amiloride on blood pressure and cardiovascular disease risk in young prehypertensives.Journal of clinical hypertension (Greenwich, Conn.) · 2014Trial
- Novel frameshift variant in the β subunit of epithelial sodium channels uncovers Liddle syndrome in a young patient with metabolic syndrome: a case report with review of literature.Endocrine journal · 2026Review
- Current understanding of ENaC regulation by P2Y2/PLC/PI(4,5)P2 pathway.Purinergic signalling · 2026Review
- Integrated mechanisms linking sodium-potassium imbalance to salt-sensitive hypertension.Physiological reports · 2025Review
- Adrenal causes of endocrine hypertension in childhood or adolescence.Journal of endocrinological investigation · 2025Review
- Myeloid Cell Glucocorticoid, Not Mineralocorticoid Receptor Signaling, Contributes to Salt-Sensitive Hypertension in Humans via Cortisol.bioRxiv : the preprint server for biology · 2024Article
- Genetic variation in salt taste receptors impact salt intake and blood pressure.Scientific reports · 2023Article
- Triamterene Functions as an Effective Nonsense Suppression Agent for MPS I-H (Hurler Syndrome).International journal of molecular sciences · 2023Article
- The epithelial sodium channel in inflammation and blood pressure modulation.Frontiers in cardiovascular medicine · 2023Review
- Soluble (Pro)Renin Receptor in Hypertension.Nephron · 2023Review
- Contributions of obesity to kidney health and disease: insights from Mendelian randomization and the human kidney transcriptomics.Cardiovascular research · 2022Article
- Hypertension and human immunodeficiency virus: A paradigm for epithelial sodium channels?Frontiers in cardiovascular medicine · 2022Review
- A narrative review of nutritional abnormalities, complications, and optimization in the cirrhotic patient.Translational gastroenterology and hepatology · 2022Review
- Antiproteinuric and Hyperkalemic Mechanisms Activated by Dual Versus Single Blockade of the RAS in Renovascular Hypertensive Rats.Frontiers in physiology · 2021Article
- CRISPR/Cas9-Mediated α-ENaC Knockout in a Murine Pancreatic β-Cell Line.Frontiers in genetics · 2021Article
- Cofilin participates in regulating alpha-epithelial sodium channel by interaction with 14-3-3 isoforms.Journal of biomedical research · 2020Article
- Interactive Actions of Aldosterone and Insulin on Epithelial NaInternational journal of molecular sciences · 2020Article
- The Role of Deubiquitinases in Vascular Diseases.Journal of cardiovascular translational research · 2020Review
- Prescription patterns of diabetes medications influencing clinical outcomes of heart failure patients with reduced ejection fraction.ESC heart failure · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This minireview examines both the basic science and clinical observations over the past 20 years to show how and why overstimulation of the amiloride-sensitive epithelial Na(+) channel (ENaC) expressed by epithelial principal cells of the renal collecting duct may be responsible for a large portion of hypertension in modern society. This idea is based on the finding that, in Liddle syndrome, a mutation of the beta- and/or gamma-subunits of ENaC produces an activated ion channel, in turn resulting in severe hypertension that is resistant to most forms of conventional antihypertensive therapy. ENaC can also be stimulated to conduct sodium by two hormones: aldosterone and insulin. These hormones are both often elevated in obese individuals with therapy-resistant hypertension. Thus, overstimulation of ENaC by metabolic abnormalities in obese individuals may be a likely cause of the hypertension that accompanies obesity. The molecular mechanisms underlying both Liddle syndrome and obesity-related hypertension are different (i.e. genetic and hormonal, respectively), but both have the same end result, namely increased ENaC activity.
Indexed as
Identifiers
What OpenQuestion holds
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.