ArticleHypertension (Dallas, Tex. : 1979)2016
Central Renin-Angiotensin System Activation and Inflammation Induced by High-Fat Diet Sensitize Angiotensin II-Elicited Hypertension.
Article in Hypertension (Dallas, Tex. : 1979), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 77 citations in OpenAlex.
- Immunology of Hypertension: Pathophysiological and Therapeutic Aspects.International journal of molecular sciences · 2025Review
- Obesity accelerates cardiovascular ageing.European heart journal · 2025Review
- The immune-microbiome axis in salt-sensitive hypertension: a focus on renal and neural mechanisms.Frontiers in physiology · 2025Review
- Role of the transcription factor NRF2 in maintaining the integrity of the Blood-Brain Barrier.Fluids and barriers of the CNS · 2024Review
- Impact of sympathetic hyperactivity induced by brain microglial activation on organ damage in sepsis with chronic kidney disease.Journal of intensive care · 2024Article
- Causal role of immune cells in hypertension: a bidirectional Mendelian randomization study.Frontiers in cardiovascular medicine · 2024Article
- SARS-CoV-2 Spike Protein S1 Exposure Increases Susceptibility to Angiotensin II-Induced Hypertension in Rats by Promoting Central Neuroinflammation and Oxidative Stress.Neurochemical research · 2023Article
- Exploring a novel therapeutic strategy: the interplay between gut microbiota and high-fat diet in the pathogenesis of metabolic disorders.Frontiers in nutrition · 2023Review
- Predator Scent-Induced Sensitization of Hypertension and Anxiety-like Behaviors.Cellular and molecular neurobiology · 2022Article
- Voluntary Exercise Prevents Hypertensive Response Sensitization Induced by Angiotensin II.Frontiers in neuroscience · 2022Article
- Sigma-1 Receptor Activation Suppresses Microglia M1 Polarization via Regulating Endoplasmic Reticulum-Mitochondria Contact and Mitochondrial Functions in Stress-Induced Hypertension Rats.Molecular neurobiology · 2021Article
- Kidney and epigenetic mechanisms of salt-sensitive hypertension.Nature reviews. Nephrology · 2021Review
- The Bidirectional Signal Communication of Microbiota-Gut-Brain Axis in Hypertension.International journal of hypertension · 2021Review
- Renal Denervation Attenuates Neuroinflammation in the Brain by Regulating Gut-Brain Axis in Rats With Myocardial Infarction.Frontiers in cardiovascular medicine · 2021Article
- Role of the renin-angiotensin system in the development of severe COVID-19 in hypertensive patients.American journal of physiology. Lung cellular and molecular physiology · 2020Review
- Salt-dependent hypertension and inflammation: targeting the gut-brain axis and the immune system with Brazilian green propolis.Inflammopharmacology · 2020Review
- Increased Susceptibility of Mice Lacking Renin-b to Angiotensin II-Induced Organ Damage.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Kinin B1 Receptor Blockade Prevents Angiotensin II-induced Neuroinflammation and Oxidative Stress in Primary Hypothalamic Neurons.Cellular and molecular neurobiology · 2020Article
- Differential effects of low-dose sacubitril and/or valsartan on renal disease in salt-sensitive hypertension.American journal of physiology. Renal physiology · 2020Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Obesity has been shown to promote renin-angiotensin system activity and inflammation in the brain and to be accompanied by increased sympathetic activity and blood pressure. Our previous studies demonstrated that administration of a subpressor dose of angiotensin (Ang) II sensitizes subsequent Ang II-elicited hypertension. The present study tested whether high-fat diet (HFD) feeding also sensitizes the Ang II-elicited hypertensive response and whether HFD-induced sensitization is mediated by an increase in renin-angiotensin system activity and inflammatory mechanisms in the brain. HFD did not increase baseline blood pressure, but enhanced the hypertensive response to Ang II compared with a normal-fat diet. The sensitization produced by the HFD was abolished by concomitant central infusions of either a tumor necrosis factor-α synthesis inhibitor, pentoxifylline, an Ang II type 1 receptor blocker, irbesartan, or an inhibitor of microglial activation, minocycline. Furthermore, central pretreatment with tumor necrosis factor-α mimicked the sensitizing action of a central subpressor dose of Ang II, whereas central pentoxifylline or minocycline abolished this Ang II-induced sensitization. Real-time quantitative reverse transcription-polymerase chain reaction analysis of lamina terminalis tissue indicated that HFD feeding, central tumor necrosis factor-α, or a central subpressor dose of Ang II upregulated mRNA expression of several components of the renin-angiotensin system and proinflammatory cytokines, whereas inhibition of Ang II type 1 receptor and of inflammation reversed these changes. The results suggest that HFD-induced sensitization of Ang II-elicited hypertension is mediated by upregulation of the brain renin-angiotensin system and of central proinflammatory cytokines.
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