ArticleAmerican journal of physiology. Renal physiology2016
Na+-sensitive elevation in blood pressure is ENaC independent in diet-induced obesity and insulin resistance.
Article in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Epithelial NaComprehensive Physiology · 2024Review
- Vascular endothelial mineralocorticoid receptors and epithelial sodium channels in metabolic syndrome and related cardiovascular disease.Journal of molecular endocrinology · 2023Review
- Pathogenesis of Hypertension in Metabolic Syndrome: The Role of Fructose and Salt.International journal of molecular sciences · 2023Review
- Effect of Chronic Western Diets on Non-Alcoholic Fatty Liver of Male Mice Modifying the PPAR-γ Pathway via miR-27b-5p Regulation.International journal of molecular sciences · 2021Article
- Review
- Obesity, kidney dysfunction and hypertension: mechanistic links.Nature reviews. Nephrology · 2019Review
- Impact of obesity as an independent risk factor for the development of renal injury: implications from rat models of obesity.American journal of physiology. Renal physiology · 2019Review
- Ion channels and transporters in diabetic kidney disease.Current topics in membranes · 2019Review
- Physiological hyperinsulinemia caused by acute hyperglycemia minimizes renal sodium loss by direct action on kidneys.American journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- Renal tubule insulin receptor modestly promotes elevated blood pressure and markedly stimulates glucose reabsorption.JCI insight · 2018Article
- Improved protocols for the study of urinary electrolyte excretion and blood pressure in rodents: use of gel food and stepwise changes in diet composition.American journal of physiology. Renal physiology · 2018Article
- Insights from direct renal insulin infusion: a new hammer for an age-old nail.American journal of physiology. Renal physiology · 2018Article
- 11β-Hydroxysteroid Dehydrogenases and Hypertension in the Metabolic Syndrome.Current hypertension reports · 2017Review
- Molecular Mechanisms of Sodium-Sensitive Hypertension in the Metabolic Syndrome.Current hypertension reports · 2017Review
- Obesity-Associated Hypertension: the Upcoming Phenotype in African-American Women.Current hypertension reports · 2017Review
- There and back again: insulin, ENaC, and the cortical collecting duct.Physiological reports · 2016Article
- Visceral adiposity syndrome.Diabetology & metabolic syndrome · 2016Review
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13 authors at 3 institutions in 1 country.
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Abstract
The majority of patients with obesity, insulin resistance, and metabolic syndrome have hypertension, but the mechanisms of hypertension are poorly understood. In these patients, impaired sodium excretion is critical for the genesis of Na(+)-sensitive hypertension, and prior studies have proposed a role for the epithelial Na(+) channel (ENaC) in this syndrome. We characterized high fat-fed mice as a model in which to study the contribution of ENaC-mediated Na(+) reabsorption in obesity and insulin resistance. High fat-fed mice demonstrated impaired Na(+) excretion and elevated blood pressure, which was significantly higher on a high-Na(+) diet compared with low fat-fed control mice. However, high fat-fed mice had no increase in ENaC activity as measured by Na(+) transport across microperfused cortical collecting ducts, electrolyte excretion, or blood pressure. In addition, we found no difference in endogenous urinary aldosterone excretion between groups on a normal or high-Na(+) diet. High fat-fed mice provide a model of metabolic syndrome, recapitulating obesity, insulin resistance, impaired natriuresis, and a Na(+)-sensitive elevation in blood pressure. Surprisingly, in contrast to previous studies, our data demonstrate that high fat feeding of mice impairs natriuresis and produces elevated blood pressure that is independent of ENaC activity and likely caused by increased Na(+) reabsorption upstream of the aldosterone-sensitive distal nephron.
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