ArticleAmerican journal of physiology. Renal physiology2011
Increased renal ENaC subunits and sodium retention in rats with chronic heart failure.
Article in American journal of physiology. Renal physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 25 citations in OpenAlex.
- Neural Upregulation of SGLT2-MAP17-PDZK1 Complex in Kidneys of Rats With Heart Failure.Hypertension (Dallas, Tex. : 1979) · 2026Article
- Activation of renal epithelial NaFrontiers in pediatrics · 2024Article
- Cardiorenal Syndrome: The Role of Neural Connections Between the Heart and the Kidneys.Circulation research · 2022Review
- Biomarkers of Volume Overload and Edema in Heart Failure With Reduced Ejection Fraction.Frontiers in cardiovascular medicine · 2022Review
- Enhanced Expression and Function of Renal SGLT2 (Sodium-Glucose Cotransporter 2) in Heart Failure: Role of Renal Nerves.Circulation. Heart failure · 2021Article
- Article
- Sympathetic Denervation Ameliorates Renal FibrosisFrontiers in immunology · 2021Article
- GLP-1 mediated diuresis and natriuresis are blunted in heart failure and restored by selective afferent renal denervation.Cardiovascular diabetology · 2020Article
- Regulating ENaC's gate.American journal of physiology. Cell physiology · 2020Review
- Transtubular potassium gradient predicts kidney function impairment after adrenalectomy in primary aldosteronism.Therapeutic advances in chronic disease · 2020Article
- Renal denervation improves sodium excretion in rats with chronic heart failure: effects on expression of renal ENaC and AQP2.American journal of physiology. Heart and circulatory physiology · 2019Article
- Does glucagon-like peptide-1 induce diuresis and natriuresis by modulating afferent renal nerve activity?American journal of physiology. Renal physiology · 2019Article
- Arterial wall hypertrophy is ameliorated by α2-adrenergic receptor antagonist or aliskiren in kidneys of angiotensinogen-knockout mice.Clinical and experimental nephrology · 2018Article
- Urinary Proteolytic Activation of Renal Epithelial Na+ Channels in Chronic Heart Failure.Hypertension (Dallas, Tex. : 1979) · 2016Article
- ANP-induced signaling cascade and its implications in renal pathophysiology.American journal of physiology. Renal physiology · 2015Review
- Renal nerves drive interstitial fibrogenesis in obstructive nephropathy.Journal of the American Society of Nephrology : JASN · 2013Article
- Neurohumoral stimulation.Heart failure clinics · 2012Review
- Clues to renal sodium retention.American journal of physiology. Renal physiology · 2011Article
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4 authors at 2 institutions in 1 country.
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Abstract
Renal tubular dysfunction could be involved in the increased sodium and water reabsorption in chronic heart failure (CHF). The goal of the present study was to examine the molecular basis for the increased renal sodium and water retention in CHF. We hypothesized that dysregulation of renal epithelial sodium channels (ENaC) could be involved in the pathogenesis of CHF. The left coronary ligation-induced model of heart failure in the rat was used. Real-time PCR and Western blot analysis indicated that the mRNA and protein abundance of α-, β-, and γ-subunits of ENaC were significantly increased by in the cortex (mRNA: α-ENaC Δ104 ± 24%, β-ENaC Δ47 ± 16%, γ-ENaC Δ55 ± 18%; protein: α-ENaC Δ114 ± 28%, β-ENaC Δ150 ± 31%, γ-ENaC Δ39 ± 5% compared with sham rats) and outer medulla (mRNA: α-ENaC Δ52 ± 18%, β-ENaC Δ38 ± 8%, γ-ENaC Δ39 ± 13%; protein: α-ENaC Δ88 ± 16%, β-ENaC Δ94 ± 28%, γ-ENaC Δ45 ± 9% compared with sham rats) of CHF compared with sham-operated rats. Immunohistochemistry microscopy confirmed the increased labeling of α-, β-, and γ-ENaC subunits in the collecting duct segments in rats with CHF. Furthermore, there was a significant increase in diuretic (7-fold compared with sham) and natriuretic responses (3-fold compared with sham) to ENaC inhibitor benzamil in the rats with CHF. Absence of renal nerves produced a greater contribution of ENaC in sodium retention in rats with CHF. These results suggest that the increased expression of renal ENaC subunits may contribute to the renal sodium and water retention observed during CHF.
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