ArticleAmerican journal of physiology. Renal physiology2016
Interleukin-6 inhibition attenuates hypertension and associated renal damage in Dahl salt-sensitive rats.
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 61 papers, 1 of them a synthesis that pooled it.
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Who cites it
61 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.
- The association between anti-inflammatory therapies and renal outcomes in patients with established cardiovascular disease or high cardiovascular risks: a meta-analysis of randomised controlled trials.Inflammopharmacology · 2025Pooled it
- The impact of dietary sodium and fructose on renal sodium handling and blood pressure in healthy adults.Physiological reports · 2025Trial
- Peptidylarginine deiminase 4 is a differential regulator of salt-sensitive and salt-resistant hypertension.iScience · 2026Article
- Review
- The expanding role of Nogo-B in hypertension: linking kidney physiology, endothelial function and inflammation.Journal of hypertension · 2026Review
- Review
- From high-salt diet to cancer immunity: gut microbiota and immune system interactions and their mechanisms.Frontiers in immunology · 2026Review
- Paradoxical sex differences in a hamster model of angiotensin II-dependent hypertension and associated renal injury.Biology of sex differences · 2025Article
- Potassium supplementation and depletion during development of salt-sensitive hypertension in male and female SS rats.JCI insight · 2025Article
- Blood-Based DNA Methylation Biomarkers to Identify Risk and Progression of Cardiovascular Disease.International journal of molecular sciences · 2025Review
- The immune-microbiome axis in salt-sensitive hypertension: a focus on renal and neural mechanisms.Frontiers in physiology · 2025Review
- Immune Mechanisms in Hypertension.Hypertension (Dallas, Tex. : 1979) · 2024Review
- Dissociation of Hypertension and Renal Damage After Cessation of High-Salt Diet in Dahl Rats.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Osteoarthritis and hypertension: observational and Mendelian randomization analyses.Arthritis research & therapy · 2024Observational
- Association of Body Mass Index with Matrix Metalloproteinase-9, Tissue Inhibitor of Metalloproteinase-1, and Interleukin-6 Based on Blood Pressure.Reports of biochemistry & molecular biology · 2024Article
- Iron Metabolism and Inflammatory Mediators in Patients with Renal Dysfunction.International journal of molecular sciences · 2024Review
- Immune cells and hypertension.Immunologic research · 2024Review
- IL-6 and diabetic kidney disease.Frontiers in immunology · 2024Review
- Mechanisms of inflammation modulation by different immune cells in hypertensive nephropathy.Frontiers in immunology · 2024Review
- Targeting inerleukin-6 for renoprotection.Frontiers in immunology · 2024Review
1 more citing papers are in PubMed but not listed here.
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6 authors at 1 institution in 1 country.
Funding
Abstract
Immune cells in the kidney are implicated in the development of hypertension and renal damage in the Dahl salt-sensitive (SS) rat. Interestingly, interleukin 6 (IL-6) mRNA is 54-fold higher in T-lymphocytes isolated from the kidney compared with circulating T-lymphocytes. The present experiments assessed the role of IL-6 in the development of SS hypertension by treating rats (n = 13-14/group) with an IL-6 neutralizing antibody or normal IgG during an 11-day period of high-salt (4.0% NaCl chow) intake. The mean arterial pressure (MAP) and urine albumin excretion rates (Ualb) were not different between the groups fed low salt (0.4% NaCl). Following 11 days of drug treatment and high salt, however, the rats receiving anti-IL-6 demonstrated a 47% reduction of IL-6 in the renal medulla compared with control SS. Moreover, the increase in MAP following 11 days of high-NaCl intake was significantly attenuated in SS administered anti-IL-6 compared with the control group (138 ± 3 vs. 149 ± 3 mmHg) as was the salt-induced increase in Ualb and glomerular and tubular damage. To investigate potential mechanisms of action, a flow cytometric analysis of immune cells in the kidney (n = 8-9/group) demonstrated that the total number of monocytes and macrophages was significantly lower in the treatment vs. the control group. The total number of T- and B-lymphocytes in the kidneys was not different between groups. These studies indicate that IL-6 production may participate in the development of SS hypertension and end-organ damage by mediating increased infiltration or proliferation of macrophages into the kidney.
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