ReviewPflugers Archiv : European journal of physiology2015
Salt controls endothelial and vascular phenotype.
Review in Pflugers Archiv : European journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 46 citations in OpenAlex.
- Beyond the guidelines: Vascular function as the central determinant and therapeutic target in hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Review
- High-Salt Diet-Induced Endothelial Dysfunction Is Mediated by Cellular Senescence.Journal of the American Heart Association · 2026Article
- HIF-1α knockdown attenuates phenotypic transformation and oxidative stress induced by high salt in human aortic vascular smooth muscle cells.Scientific reports · 2024Article
- Review
- Erythrocyte glycocalyx sensitivity to sodium is associated with salt sensitivity of blood pressure in women but not men.Frontiers in nutrition · 2024Article
- Salt Behind the Scenes of Systemic Lupus Erythematosus and Rheumatoid Arthritis.Current nutrition reports · 2023Review
- Endothelial dysfunction as a factor leading to arterial hypertension.Pediatric nephrology (Berlin, Germany) · 2023Article
- Emerging Role of Sodium-Glucose Co-Transporter 2 Inhibitors for the Treatment of Chronic Kidney Disease.International journal of nephrology and renovascular disease · 2023Review
- The impact of progredient vessel and tissue stiffening for the development of metabolic syndrome.Pflugers Archiv : European journal of physiology · 2022Review
- The Potential Roles of Osmotic and Nonosmotic Sodium Handling in Mediating the Effects of Sodium-Glucose Cotransporter 2 Inhibitors on Heart Failure.Journal of cardiac failure · 2021Review
- High NaBiomedicines · 2021Review
- Endothelial Dysfunction in Diabetes.Biomedicines · 2020Review
- Sodium Intake and Target Organ Damage in Hypertension-An Update about the Role of a Real Villain.International journal of environmental research and public health · 2020Review
- The association between salt intake and arterial stiffness is influenced by a sex-specific mediating effect through blood pressure in normotensive adults: The ELSA-Brasil study.Journal of clinical hypertension (Greenwich, Conn.) · 2019Article
- The role of endothelial glycocalyx in health and disease.Clinical kidney journal · 2019Article
- The Absence of Endothelial Sodium Channel α (αENaC) Reduces Renal Ischemia/Reperfusion Injury.International journal of molecular sciences · 2019Article
- Article
- New insights into arterial stiffening: does sex matter?American journal of physiology. Heart and circulatory physiology · 2018Review
- Inflammasome-Independent NALP3 Contributes to High-Salt Induced Endothelial Dysfunction.Frontiers in pharmacology · 2018Article
- Salt-induced NaPflugers Archiv : European journal of physiology · 2017Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High salt (NaCl) intake promotes the development of vascular diseases independent of a rise in blood pressure, whereas reduction of salt consumption has beneficial effects for the arterial system. This article summarizes our current understanding of the molecular mechanisms of high salt-induced alterations of the endothelial phenotype, the impact of the individual endothelial genotype, and the overall vascular phenotype. We focus on the endothelial Na(+) channel (EnNaC)-controlled nanomechanical properties of the endothelium, since high Na(+) leads to an EnNaC-induced Na(+)-influx and subsequent stiffening of endothelial cells. The mechanical stiffness of the endothelial cell (i.e., the endothelial phenotype) plays a crucial role as it controls the production of the endothelium-derived vasodilator nitric oxide (NO) which directly affects the tone of the vascular smooth muscle cells. In contrast to soft endothelial cells, stiff endothelial cells release reduced amounts of NO, the hallmark of endothelial dysfunction. This endothelium-born process is followed by the development of arterial stiffness (i.e., the vascular phenotype), predicting the development of vascular end-organ damage such as myocardial infarction, stroke, and renal impairment. In this context, we outline the potential clinical implication of direct (amiloride) and indirect (spironolactone) EnNaC inhibition on vascular function. However, interindividual differences exist in the response to high salt intake which involves different endothelial genotypes. Thus, selected genes and genetic variants contributing to the development of salt-induced endothelial dysfunction and hypertension are discussed. In this review, we focus on the role of salt in endothelial and vascular (dys)function and the link between salt-induced changes of the endothelial and vascular phenotype and its clinical implications.
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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.