ArticlePflugers Archiv : European journal of physiology2016
The mineralocorticoid receptor (MR) regulates ENaC but not NCC in mice with random MR deletion.
Article in Pflugers Archiv : European journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 54 citations in OpenAlex.
- Intrarenal Hemodynamic Mechanisms of Kidney Protection by Nonsteroidal Mineralocorticoid Receptor Antagonists.Endocrinology and metabolism (Seoul, Korea) · 2026Review
- The Story of Aldosterone Escape.Journal of the American Society of Nephrology : JASN · 2026Review
- Sodium Chloride Cotransporter in Hypertension.Biomedicines · 2024Review
- Aldosterone-independent regulation of K + secretion in the distal nephron.Current opinion in nephrology and hypertension · 2024Review
- Navigating the multifaceted intricacies of the NaPhysiological reviews · 2024Review
- Modifying Dietary Sodium and Potassium Intake: An End to the 'Salt Wars'?Hypertension (Dallas, Tex. : 1979) · 2024Review
- Thirty years of the NaCl cotransporter: from cloning to physiology and structure.American journal of physiology. Renal physiology · 2023Review
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- Kir4.2 mediates proximal potassium effects on glutaminase activity and kidney injury.Cell reports · 2022Article
- Blood pressure effects of sodium transport along the distal nephron.Kidney international · 2022Review
- In Primary Aldosteronism Acute Potassium Chloride Supplementation Suppresses Abundance and Phosphorylation of the Sodium-Chloride Cotransporter.Kidney360 · 2022Article
- Regulation of distal tubule sodium transport: mechanisms and roles in homeostasis and pathophysiology.Pflugers Archiv : European journal of physiology · 2022Review
- Potassium homeostasis: sensors, mediators, and targets.Pflugers Archiv : European journal of physiology · 2022Review
- Article
- Regulation of Blood Pressure and Salt Balance By Pendrin-Positive Intercalated Cells: Donald Seldin Lecture 2020.Hypertension (Dallas, Tex. : 1979) · 2022Review
- Molecular mechanisms for the modulation of blood pressure and potassium homeostasis by the distal convoluted tubule.EMBO molecular medicine · 2022Review
- HIV-1 Vpr suppresses expression of the thiazide-sensitive sodium chloride co-transporter in the distal convoluted tubule.PloS one · 2022Article
- Dissecting the Effects of Aldosterone and Hypokalemia on the Epithelial NaFrontiers in physiology · 2022Article
- WNK4 kinase: from structure to physiology.American journal of physiology. Renal physiology · 2021Review
- The WNK signaling pathway and salt-sensitive hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2020Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aldosterone binds to the mineralocorticoid receptor (MR) and increases renal Na(+) reabsorption via up-regulation of the epithelial Na(+) channel (ENaC) and the Na(+)-K(+)-ATPase in the collecting system (CS) and possibly also via the NaCl cotransporter (NCC) in the distal convoluted tubule (DCT). However, whether aldosterone directly regulates NCC via MR or indirectly through systemic alterations remains controversial. We used mice with deletion of MR in ∼20 % of renal tubule cells (MR/X mice), in which MR-positive (MR(wt)) and -negative (MR(ko)) cells can be studied side-by-side in the same physiological context. Adult MR/X mice showed similar mRNA and protein levels of renal ion transport proteins to control mice. In MR/X mice, no differences in NCC abundance and phosphorylation was seen between MR(wt) and MR(ko) cells and dietary Na(+) restriction up-regulated NCC to similar extent in both groups of cells. In contrast, MR(ko) cells in the CS did not show any detectable alpha-ENaC abundance or apical targeting of ENaC neither on control diet nor in response to dietary Na(+) restriction. Furthermore, Na(+)-K(+)-ATPase expression was unaffected in MR(ko) cells of the DCT, while it was lost in MR(ko) cells of the CS. In conclusion, MR is crucial for ENaC and Na(+)-K(+)-ATPase regulation in the CS, but is dispensable for NCC and Na(+)-K(+)-ATPase regulation in the DCT.
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