ArticleAmerican journal of physiology. Renal physiology2015
Acute effects of aldosterone on the epithelial Na channel in rat kidney.
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 31 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
31 citing papers in PubMed, 48 citations in OpenAlex.
- Low-Salt Diet Induces Claudin-3 Expression and Drives Adaptive Changes in Collecting Duct of Claudin-3-Deficient Mice.Acta physiologica (Oxford, England) · 2026Article
- Kinetics of aldosterone-dependent ENaC trafficking in the kidney.The Journal of general physiology · 2025Article
- Salt sensitivity of blood pressure: mechanisms and sex-specific differences.Nature reviews. Cardiology · 2025Review
- Epithelial Na+ Channels, Immune Cells, and Salt.Annual review of physiology · 2025Review
- ENaCγ in Urinary Extracellular Vesicles as an Indicator of MR Signaling in Primary Aldosteronism.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Loss of the alpha subunit distal furin cleavage site blunts ENaC activation following NaThe Journal of physiology · 2024Article
- Epithelial NaComprehensive Physiology · 2024Review
- Dietary sodium alters aldosterone's effect on renal sodium transporter expression and distal convoluted tubule remodelling.The Journal of physiology · 2024Article
- Aldosterone Antagonism Is More Effective at Reducing Blood Pressure and Excessive Renal ENaC Activity in AngII-Infused Female Rats Than in Males.Hypertension (Dallas, Tex. : 1979) · 2023Article
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- Bile acids regulate the epithelial NaThe Journal of physiology · 2022Article
- Renal NOXA1/NOX1 Signaling Regulates Epithelial Sodium Channel and Sodium Retention in Angiotensin II-induced Hypertension.Antioxidants & redox signaling · 2022Article
- Activation by cleavage of the epithelial NaeLife · 2022Article
- Epithelial Sodium Channel and Salt-Sensitive Hypertension.Hypertension (Dallas, Tex. : 1979) · 2021Review
- Myristoylated alanine-rich C kinase substrate-like protein-1 regulates epithelial sodium channel activity in renal distal convoluted tubule cells.American journal of physiology. Cell physiology · 2020Article
- Aldosterone-dependent and -independent regulation of NaAmerican journal of physiology. Renal physiology · 2020Article
- Upregulation of Claudin-7 Expression by Angiotensin II in Colonic Epithelial Cells of Mice Fed with NaCl-Depleted Diets.International journal of molecular sciences · 2020Article
- Regulating ENaC's gate.American journal of physiology. Cell physiology · 2020Review
- Murine epithelial sodium (NaThe Journal of biological chemistry · 2019Article
- The N terminus of α-ENaC mediates ENaC cleavage and activation by furin.The Journal of general physiology · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The acute effects of aldosterone administration on epithelial Na channels (ENaC) in rat kidney were examined using electrophysiology and immunodetection. Animals received a single injection of aldosterone (20 μg/kg body wt), which reduced Na excretion over the next 3 h. Channel activity was assessed in principal cells of cortical collecting ducts as amiloride-sensitive whole cell clamp current (INa). INa averaged 100 pA/cell, 20-30% of that reported for the same preparation under conditions of chronic stimulation. INa was negligible in control animals that did not receive hormone. The acute physiological response correlated with changes in ENaC processing and trafficking. These effects included increases in the cleaved forms of α-ENaC and γ-ENaC, assessed by Western blot, and increases in the surface expression of β-ENaC and γ-ENaC measured after surface protein biotinylation. These changes were qualitatively and quantitatively similar to those of chronic stimulation. This suggests that altered trafficking to or from the apical membrane is an early response to the hormone and that later increases in channel activity require stimulation of channels residing at the surface.
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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.