ArticleJournal of the American Society of Nephrology : JASN2014
Colon-specific deletion of epithelial sodium channel causes sodium loss and aldosterone resistance.
Article in Journal of the American Society of Nephrology : JASN, 2014. 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
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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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Who cites it
53 citing papers in PubMed, 78 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
- Article
- Gut-Heart Axis: The Role of Gut Microbiota and Metabolites in Heart Failure.Circulation research · 2025Review
- Diet-Microbiota-Host Interactions in Regulation of Cardiometabolic Homeostasis: Emerging Mechanisms and Therapeutic Potential.Microbiota and host · 2025Article
- Epithelial Na+ Channels, Immune Cells, and Salt.Annual review of physiology · 2025Review
- Loss of the alpha subunit distal furin cleavage site blunts ENaC activation following NaThe Journal of physiology · 2024Article
- Altered Plasma Membrane Lipid Composition in Hypertensive Neutrophils Impacts Epithelial Sodium Channel (ENaC) Endocytosis.International journal of molecular sciences · 2024Article
- Epithelial NaComprehensive Physiology · 2024Review
- Tmprss2 maintains epithelial barrier integrity and transepithelial sodium transport.Life science alliance · 2024Article
- Bioinformatics Prediction for Network-Based Integrative Multi-Omics Expression Data Analysis in Hirschsprung Disease.Biomolecules · 2024Article
- Proteolytic Activation of the Epithelial Sodium Channel (ENaC): Its Mechanisms and Implications.International journal of molecular sciences · 2023Review
- Mice lacking γENaC palmitoylation sites maintain benzamil-sensitive Na+ transport despite reduced channel activity.JCI insight · 2023Article
- IntestinalJournal of geriatric cardiology : JGC · 2023Article
- Article
- Predisposing factors for high output stoma in patients with a diverting loop ileostomy after colorectal surgeries.Annals of coloproctology · 2023Article
- Circadian rhythms in colonic function.Frontiers in physiology · 2023Review
- Rare Variants in Genes Encoding Subunits of the Epithelial NaHypertension (Dallas, Tex. : 1979) · 2022Article
- Elevated intracellular NaProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Kidney-Specific CAP1/Prss8-Deficient Mice Maintain ENaC-Mediated Sodium Balance through an Aldosterone Independent Pathway.International journal of molecular sciences · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aldosterone promotes electrogenic sodium reabsorption through the amiloride-sensitive epithelial sodium channel (ENaC). Here, we investigated the importance of ENaC and its positive regulator channel-activating protease 1 (CAP1/Prss8) in colon. Mice lacking the αENaC subunit in colonic superficial cells (Scnn1a(KO)) were viable, without fetal or perinatal lethality. Control mice fed a regular or low-salt diet had a significantly higher amiloride-sensitive rectal potential difference (∆PDamil) than control mice fed a high-salt diet. In Scnn1a(KO) mice, however, this salt restriction-induced increase in ∆PDamil did not occur, and the circadian rhythm of ∆PDamil was blunted. Plasma and urinary sodium and potassium did not change with regular or high-salt diets or potassium loading in control or Scnn1a(KO) mice. However, Scnn1a(KO) mice fed a low-salt diet lost significant amounts of sodium in their feces and exhibited high plasma aldosterone and increased urinary sodium retention. Mice lacking the CAP1/Prss8 in colonic superficial cells (Prss8(KO)) were viable, without fetal or perinatal lethality. Compared with controls, Prss8(KO) mice fed regular or low-salt diets exhibited significantly reduced ∆PDamil in the afternoon, but the circadian rhythm was maintained. Prss8(KO) mice fed a low-salt diet also exhibited sodium loss through feces and higher plasma aldosterone levels. Thus, we identified CAP1/Prss8 as an in vivo regulator of ENaC in colon. We conclude that, under salt restriction, activation of the renin-angiotensin-aldosterone system in the kidney compensated for the absence of ENaC in colonic surface epithelium, leading to colon-specific pseudohypoaldosteronism type 1 with mineralocorticoid resistance without evidence of impaired potassium balance.
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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.