ArticleAmerican journal of physiology. Renal physiology2015
Activation of ENaC by AVP contributes to the urinary concentrating mechanism and dilution of plasma.
Article in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 31 citations in OpenAlex.
- Effect of 3% saline and furosemide on biomarkers of kidney injury and renal tubular function and GFR in healthy subjects - a randomized controlled trial.BMC nephrology · 2019Trial
- ENaC phosphorylation facilitates ankyrin-3 interaction critical for renal sodium balance.PNAS nexus · 2026Article
- Syndrome of Inappropriate Antidiuresis.Journal of the American Society of Nephrology : JASN · 2025Review
- Syndrome of Inappropriate Antidiuresis: From Pathophysiology to Management.Endocrine reviews · 2023Review
- Bile acid receptors and renal regulation of water homeostasis.Frontiers in physiology · 2023Review
- Blood pressure effects of sodium transport along the distal nephron.Kidney international · 2022Review
- Chronic activation of vasopressin-2 receptors induces hypertension in Liddle mice by promoting NaAmerican journal of physiology. Renal physiology · 2022Article
- Renal water transport in health and disease.Pflugers Archiv : European journal of physiology · 2022Review
- Article
- Pathophysiology and genetics of salt-sensitive hypertension.Frontiers in physiology · 2022Review
- Mechanisms and consequences of casein kinase II and ankyrin-3 regulation of the epithelial NaScientific reports · 2021Article
- Stimulation of the Epithelial NaFrontiers in physiology · 2021Article
- Article
- Interactive Actions of Aldosterone and Insulin on Epithelial NaInternational journal of molecular sciences · 2020Article
- Sickle cell disease up-regulates vasopressin, aquaporin 2, urea transporter A1, Na-K-Cl cotransporter 2, and epithelial Na channels in the mouse kidney medulla despite compromising urinary concentration ability.Physiological reports · 2019Article
- Thirst Increases Chorda Tympani Responses to Sodium Chloride.Chemical senses · 2017Article
- Involvement of ENaC in the development of salt-sensitive hypertension.American journal of physiology. Renal physiology · 2017Review
- ENaC activity in the cortical collecting duct of HKαAmerican journal of physiology. Renal physiology · 2017Article
- Gastrointestinal-Renal Axis: Role in the Regulation of Blood Pressure.Journal of the American Heart Association · 2017Review
- Gastrorenal Axis.Hypertension (Dallas, Tex. : 1979) · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Arginine vasopressin (AVP) activates the epithelial Na(+) channel (ENaC). The physiological significance of this activation is unknown. The present study tested if activation of ENaC contributes to AVP-sensitive urinary concentration. Consumption of a 3% NaCl solution induced hypernatremia and plasma hypertonicity in mice. Plasma AVP concentration and urine osmolality increased in hypernatremic mice in an attempt to compensate for increases in plasma tonicity. ENaC activity was elevated in mice that consumed 3% NaCl solution compared with mice that consumed a diet enriched in Na(+) with ad libitum tap water; the latter diet does not cause hypernatremia. To determine whether the increase in ENaC activity in mice that consumed 3% NaCl solution served to compensate for hypernatremia, mice were treated with the ENaC inhibitor benzamil. Coadministration of benzamil with 3% NaCl solution decreased urinary osmolality and increased urine flow so that urinary Na(+) excretion increased with no effect on urinary Na(+) concentration. This decrease in urinary concentration further increased plasma Na(+) concentration, osmolality, and AVP concentration in these already hypernatremic mice. Benzamil similarly compromised urinary concentration in water-deprived mice and in mice treated with desmopressin. These results demonstrate that stimulation of ENaC by AVP plays a critical role in water homeostasis by facilitating urinary concentration, which can compensate for hypernatremia or exacerbate hyponatremia. The present findings are consistent with ENaC in addition to serving as a final effector of the renin-angiotensin-aldosterone system and blood pressure homeostasis, also playing a key role in water homeostasis by regulating urine concentration and dilution of plasma.
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.