ArticleJournal of the American Society of Nephrology : JASN2010
Sodium and potassium balance depends on αENaC expression in connecting tubule.
Article in Journal of the American Society of Nephrology : JASN, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 91 citations in OpenAlex.
- Validation and Assessment of Three Methods to Estimate 24-h Urinary Sodium Excretion from Spot Urine Samples in High-Risk Elder Patients of Stroke from the Rural Areas of Shaanxi Province.International journal of environmental research and public health · 2017Trial
- Mechanosensitive Ion Channels: Their Physiological Importance and Potential Key Role in Cancer.International journal of molecular sciences · 2023Review
- The Post-Translational Modification Networking in WNK-Centric Hypertension Regulation and Electrolyte Homeostasis.Biomedicines · 2022Review
- Epithelial Sodium Channel Alpha Subunit (αENaC) Is Associated with Inverse Salt Sensitivity of Blood Pressure.Biomedicines · 2022Article
- Dissecting the Effects of Aldosterone and Hypokalemia on the Epithelial NaFrontiers in physiology · 2022Article
- Salt sensitivity of volume and blood pressure in a mouse with globally reduced ENaC γ-subunit expression.American journal of physiology. Renal physiology · 2021Article
- Selective Deletion of the Mechanistic Target of Rapamycin From the Renal Collecting Duct Principal Cell in Mice Down-Regulates the Epithelial Sodium Channel.Frontiers in physiology · 2021Article
- Paraoxonase 3 functions as a chaperone to decrease functional expression of the epithelial sodium channel.The Journal of biological chemistry · 2020Article
- Lack of Renal Tubular Glucocorticoid Receptor Decreases the Thiazide-Sensitive NaFrontiers in physiology · 2019Article
- RNA sequencing of kidney distal tubule cells reveals multiple mediators of chronic aldosterone action.Physiological genomics · 2018Article
- Severe hyperkalemia is rescued by low-potassium diet in renal βENaC-deficient mice.Pflugers Archiv : European journal of physiology · 2017Article
- Constitutively Active SPAK Causes Hyperkalemia by Activating NCC and Remodeling Distal Tubules.Journal of the American Society of Nephrology : JASN · 2017Article
- Diurnal variation of urinary sodium-to-potassium ratio in free-living Japanese individuals.Hypertension research : official journal of the Japanese Society of Hypertension · 2017Article
- Aldosterone Modulates the Association between NCC and ENaC.Scientific reports · 2017Article
- Role of adenylyl cyclase 6 in the development of lithium-induced nephrogenic diabetes insipidus.JCI insight · 2017Article
- The sodium chloride cotransporter (NCC) and epithelial sodium channel (ENaC) associate.The Biochemical journal · 2016Article
- The function and regulation of acid-sensing ion channels (ASICs) and the epithelial Na(+) channel (ENaC): IUPHAR Review 19.British journal of pharmacology · 2016Review
- Renal tubular SGK1 deficiency causes impaired K+ excretion via loss of regulation of NEDD4-2/WNK1 and ENaC.American journal of physiology. Renal physiology · 2016Article
- Severe Salt-Losing Syndrome and Hyperkalemia Induced by Adult Nephron-Specific Knockout of the Epithelial Sodium Channel α-Subunit.Journal of the American Society of Nephrology : JASN · 2016Article
- Acetazolamide Attenuates Lithium-Induced Nephrogenic Diabetes Insipidus.Journal of the American Society of Nephrology : JASN · 2016Article
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Authors and funding
11 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in α, β, or γ subunits of the epithelial sodium channel (ENaC) can downregulate ENaC activity and cause a severe salt-losing syndrome with hyperkalemia and metabolic acidosis, designated pseudohypoaldosteronism type 1 in humans. In contrast, mice with selective inactivation of αENaC in the collecting duct (CD) maintain sodium and potassium balance, suggesting that the late distal convoluted tubule (DCT2) and/or the connecting tubule (CNT) participates in sodium homeostasis. To investigate the relative importance of ENaC-mediated sodium absorption in the CNT, we used Cre-lox technology to generate mice lacking αENaC in the aquaporin 2-expressing CNT and CD. Western blot analysis of microdissected cortical CD (CCD) and CNT revealed absence of αENaC in the CCD and weak αENaC expression in the CNT. These mice exhibited a significantly higher urinary sodium excretion, a lower urine osmolality, and an increased urine volume compared with control mice. Furthermore, serum sodium was lower and potassium levels were higher in the genetically modified mice. With dietary sodium restriction, these mice experienced significant weight loss, increased urinary sodium excretion, and hyperkalemia. Plasma aldosterone levels were significantly elevated under both standard and sodium-restricted diets. In summary, αENaC expression within the CNT/CD is crucial for sodium and potassium homeostasis and causes signs and symptoms of pseudohypoaldosteronism type 1 if missing.
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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.