ArticleInternational archives of medicine2009
Regulation of the epithelial sodium channel [ENaC] in kidneys of salt-sensitive Dahl rats: insights on alternative splicing.
Article in International archives of medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Common variants in epithelial sodium channel genes contribute to salt sensitivity of blood pressure: The GenSalt study.Circulation. Cardiovascular genetics · 2011Trial
- Effects of a high-salt diet on MAP and expression levels of renal ENaCs and aquaporins in SHR.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Article
- High Salt Diet Affects Renal Sodium Excretion and ERRα Expression.International journal of molecular sciences · 2016Article
- Gain-of-Function Mutation W493R in the Epithelial Sodium Channel Allosterically Reconfigures Intersubunit Coupling.The Journal of biological chemistry · 2016Article
- Role of precursor mRNA splicing in nutrient-induced alterations in gene expression and metabolism.The Journal of nutrition · 2015Review
- Associations of epithelial sodium channel genes with blood pressure: the GenSalt study.Journal of human hypertension · 2015Article
- Connecting tubule glomerular feedback in hypertension.Hypertension (Dallas, Tex. : 1979) · 2013Article
- ENaCs and ASICs as therapeutic targets.American journal of physiology. Cell physiology · 2012Review
- The Alternatively Spliced Form "b" of the Epithelial Sodium Channel α subunit (α ENaC): Any Prior Evidence of its Existence?Clinical Medicine Insights. Cardiology · 2010Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
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Abstract
The epithelial sodium channel [ENaC] is critical for the maintenance of sodium balance, extracellular fluid volume and long term blood pressure control. Monogenic disorders causing ENaC hyperactivity have led to a severe form of hereditary hypertension in humans, known as Liddle's syndrome. Similarly, in animal models, ENaC hyperactivity has been well documented in kidneys of salt-sensitive [S] Dahl rats [a genetic model of salt-sensitive hypertension] versus their normotensive control [Dahl salt-resistant [R] rats]. The purpose of the present review is to highlight the differential regulation of ENaC in kidneys of Dahl S versus R rats. A systematic overview of the putative role of alternative splicing of the main alpha subunit of ENaC [alpha ENaC] in modulating ENaC expression in kidneys of Dahl rats will be discussed. Finally, a better understanding of the meaningful contribution of ENaC in the pathogenesis of salt-sensitive hypertension will be achieved upon completion of this review.
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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.