ArticleHypertension (Dallas, Tex. : 1979)2024
IL-1R Mediated Activation of Renal Sensory Nerves in DOCA-Salt Hypertension.
Article in Hypertension (Dallas, Tex. : 1979), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Gastrodin Ameliorates Blood Pressure by Targeting the PPAR-γ/NF-κB/NLRP3 Signaling Axis in the Hypothalamic Paraventricular Nucleus.Cardiovascular toxicology · 2026Article
- Preferential renal tubular injury and increased renal sympathetic activity occur during the early stages of DOCA-salt hypertension in male rats.Physiological reports · 2026Article
- The sympathetic nervous system in the pathophysiology of hypertension: Mechanistic insights and therapeutic implications.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Review
- Animal models of hypertension and concurrent organs injury.Animal models and experimental medicine · 2025Review
- Renal interoception: form, function, and open questions.Current opinion in neurobiology · 2025Review
- A Novel Catheter-Based Method for Denervation of Afferent Renal Nerves in Sheep.Cardiovascular engineering and technology · 2025Article
- Clonal Hematopoiesis Increases Hypertension and Sympathetic Activity and Is Reversed by Renal Denervation.Hypertension (Dallas, Tex. : 1979) · 2025Article
- The organum vasculosum of the lamina terminalis contributes to neurohumoral mechanisms of renal vascular hypertension.American journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
- 2-Kidney-1-clip hypertension is not attenuated in mice lacking the transient receptor potential vanilloid type 1 (TRPV1) channel.Frontiers in physiology · 2025Article
- The immune-microbiome axis in salt-sensitive hypertension: a focus on renal and neural mechanisms.Frontiers in physiology · 2025Review
- Renal nerves in physiology, pathophysiology and interoception.Nature reviews. Nephrology · 2025Review
- Afferent innervation of the kidney: projections to and processing in the central nervous system.Frontiers in physiology · 2025Review
- 8-Aminopurines: A Promising New Direction for Purine-Based Therapeutics.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Renal interoception in health and disease.Autonomic neuroscience : basic & clinical · 2024Review
- 8-Aminoguanine and its actions in the metabolic syndrome.Scientific reports · 2024Article
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6 authors.
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Abstract
backgroundClinical trials of renal denervation for the treatment of hypertension have shown a variety of off-target improvements in conditions associated with sympathetic overactivity. This may be due to the ablation of sympathoexcitatory afferent renal nerves, which are overactive under conditions of renal inflammation. Renal IL (interleukin)-1β is elevated in the deoxycorticosterone acetate-salt model of hypertension, and its activity may be responsible for the elevation in afferent renal nerve activity and arterial pressure.
methodsContinuous blood pressure recording of deoxycorticosterone acetate-salt mice with IL-1R (IL-1 receptor) knockout or antagonism was used individually and combined with afferent renal denervation (ARDN) to assess mechanistic overlap. Protein quantification and histological analysis of kidneys were performed to characterize renal inflammation.
resultsARDN attenuated deoxycorticosterone acetate-salt hypertension (-20±2-Δmm Hg mean arterial pressure [MAP] relative to control at study end) to a similar degree as total renal denervation (-21±2-Δmm Hg MAP), IL-1R knockout (-16±4-Δmm Hg MAP), or IL-1R antagonism (-20±3-Δmm Hg MAP). The combination of ARDN with knockout (-18±2-Δmm Hg MAP) or antagonism (-19±4-Δmm Hg MAP) did not attenuate hypertension any further than ARDN alone. IL-1R antagonism was found to have an acute depressor effect (-15±3-Δmm Hg MAP, day 10) in animals with intact renal nerves but not those with ARDN.
conclusionsThese findings suggest that IL-1R signaling is partially responsible for the elevated afferent renal nerve activity, which stimulates central sympathetic outflow to drive deoxycorticosterone acetate-salt hypertension.
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