ArticleThe Journal of biological chemistry2012
Angiotensin II increases activity of the epithelial Na+ channel (ENaC) in distal nephron additively to aldosterone.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
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Who cites it
99 citing papers in PubMed, 146 citations in OpenAlex.
- Upregulated Renal Mineralocorticoid Receptor and 11β-Hydroxysteroid Dehydrogenase Type 2 Are Associated with KInternational journal of molecular sciences · 2026Article
- ENaC processing in rat kidney: effects of salt loading and ADH.American journal of physiology. Renal physiology · 2026Article
- Ovarian hormones moderate systolic hypertension in femaleAmerican journal of physiology. Renal physiology · 2026Article
- Ovarian Hormones Moderate Systolic Hypertension in FemalebioRxiv : the preprint server for biology · 2025Article
- Hypomagnesaemia-associated hypokalaemia requires activation of both ENaC and ROMK.The Journal of physiology · 2025Article
- SARS-CoV-2 N protein induces hypokalemia in acute kidney injury mice via ENaC-dependent mechanism.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Angiotensin II-Type-1a Receptor and Renal K + Wasting during Overnight Low-Na + Intake.Journal of the American Society of Nephrology : JASN · 2024Article
- A Possible Link between Cell Plasticity and Renin Expression in the Collecting Duct: A Narrative Review.International journal of molecular sciences · 2024Review
- HIV-Associated Hypertension: Risks, Mechanisms, and Knowledge Gaps.Circulation research · 2024Review
- Human soluble prorenin receptor expressed in mouse renal collecting duct shows sex-specific effect on cardiorenal function.American journal of physiology. Renal 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
- Proteolytic Activation of the Epithelial Sodium Channel (ENaC): Its Mechanisms and Implications.International journal of molecular sciences · 2023Review
- Fibrinolytic system and COVID-19: From an innovative view of epithelial ion transport.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Review
- Review
- Blood pressure effects of sodium transport along the distal nephron.Kidney international · 2022Review
- NOXA1-dependent NADPH oxidase 1 signaling mediates angiotensin II activation of the epithelial sodium channel.American journal of physiology. Renal physiology · 2022Article
- Bile acids regulate the epithelial NaThe Journal of physiology · 2022Article
- Interleukin 6 mediated activation of the mineralocorticoid receptor in the aldosterone-sensitive distal nephron.American journal of physiology. Cell physiology · 2022Article
39 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Dietary salt intake controls epithelial Na+ channel (ENaC)-mediated Na+ reabsorption in the distal nephron by affecting status of the renin-angiotensin-aldosterone system (RAAS). Whereas regulation of ENaC by aldosterone is generally accepted, little is known about whether other components of RAAS, such as angiotensin II (Ang II), have nonredundant to aldosterone-stimulatory actions on ENaC. We combined patch clamp electrophysiology and immunohistochemistry in freshly isolated split-opened distal nephrons of mice to determine the mechanism and molecular signaling pathway of Ang II regulation of ENaC. We found that Ang II acutely increases ENaC Po, whereas prolonged exposure to Ang II also induces translocation of α-ENaC toward the apical membrane in situ. Ang II actions on ENaC Po persist in the presence of saturated mineralocorticoid status. Moreover, aldosterone fails to stimulate ENaC acutely, suggesting that Ang II and aldosterone have different time frames of ENaC activation. AT1 but not AT2 receptors mediate Ang II actions on ENaC. Unlike its effect in vasculature, Ang II did not increase [Ca2+]i in split-opened distal nephrons as demonstrated using ratiometric Fura-2-based microscopy. However, application of Ang II to mpkCCDc14 cells resulted in generation of reactive oxygen species, as probed with fluorescent methods. Consistently, inhibiting NADPH oxidase with apocynin abolished Ang II-mediated increases in ENaC Po in murine distal nephron. Therefore, we concluded that Ang II directly regulates ENaC activity in the distal nephron, and this effect complements regulation of ENaC by aldosterone. We propose that stimulation of AT1 receptors with subsequent activation of NADPH oxidase signaling pathway mediates Ang II actions on ENaC.
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