ArticleCellular and molecular neurobiology2020
Kinin B1 Receptor Blockade Prevents Angiotensin II-induced Neuroinflammation and Oxidative Stress in Primary Hypothalamic Neurons.
Article in Cellular and molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- ACE2: Friend or Foe in Post-COVID-19 Neurodegeneration?International journal of molecular sciences · 2025Review
- The application of telmisartan in central nervous system disorders.Pharmacological reports : PR · 2025Review
- Targeting Kinin B1R Attenuates Hypertension Through AT1R-Dependent Mechanisms.Circulation research · 2025Article
- Kinin B1 receptor mediates acute cardiovascular and neural responses following cannabinoid receptor 1 activation in conscious male mice.Physiological reports · 2025Article
- Article
- Function and structure of bradykinin receptor 2 for drug discovery.Acta pharmacologica Sinica · 2023Review
- Kinin B1 Receptor Mediates Bidirectional Interaction between Neuroinflammation and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2023Article
- Cardiomyocyte-specific deletion of TLR4 attenuates angiotensin II-induced hypertension and cardiac remodeling.Frontiers in cardiovascular medicine · 2023Article
- Bradykinin-target therapies in SARS-CoV-2 infection: current evidence and perspectives.Naunyn-Schmiedeberg's archives of pharmacology · 2022Review
- Cryo-EM structures of human bradykinin receptor-GNature communications · 2022Article
- Molecular pathways involved in COVID-19 and potential pathway-based therapeutic targets.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
- Kinin B1R Activation Induces Endoplasmic Reticulum Stress in Primary Hypothalamic Neurons.Frontiers in pharmacology · 2022Article
- Mitochondria-Endoplasmic Reticulum Crosstalk in Parkinson's Disease: The Role of Brain Renin Angiotensin System Components.Biomolecules · 2021Review
- Hypothalamic kinin B1 receptor mediates orexin system hyperactivity in neurogenic hypertension.Scientific reports · 2021Article
- Review
- Interactions amongst inflammation, renin-angiotensin-aldosterone and kallikrein-kinin systems: suggestive approaches for COVID-19 therapy.The journal of venomous animals and toxins including tropical diseases · 2021Review
- Kinin B1 Receptor Mediates Renal Injury and Remodeling in Hypertension.Frontiers in medicine · 2021Article
- Activation of Kinin B1R Upregulates ADAM17 and Results in ACE2 Shedding in Neurons.International journal of molecular sciences · 2020Article
- Angiotensin-Converting Enzyme Inhibitor Protects Against Cisplatin Nephrotoxicity by Modulating Kinin B1 Receptor Expression and Aminopeptidase P Activity in Mice.Frontiers in molecular biosciences · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Neuroinflammation has become an important underlying factor in many cardiovascular disorders, including hypertension. Previously we showed that elevated angiotensin II (Ang II) and angiotensin II type I receptor (AT1R) expression levels can increase neuroinflammation leading to hypertension. We also found that kinin B1 receptor (B1R) expression increased in the hypothalamic paraventricular neurons resulting in neuroinflammation and oxidative stress in neurogenic hypertension. However, whether there are any potential interactions between AT1R and B1R in neuroinflammation is not clear. In the present study, we aimed to determine whether Ang II-mediated effects on inflammation and oxidative stress are mediated by the activation of B1R in mouse neonatal primary hypothalamic neuronal cultures. Gene expression and immunostaining revealed that both B1R and AT1R are expressed on primary hypothalamic neurons. Ang II stimulation significantly increased the expression of B1R, decreased mitochondrial respiration, increased the expression of two NADPH oxidase subunits (Nox2 and Nox4), increased the oxidative potential, upregulated several proinflammatory genes (IL-1β, IL-6, and TNFα), and increased NF-kB p65 DNA binding activity. These changes were prevented by pretreatment with the B1R-specific peptide antagonist, R715. In summary, our study demonstrates a causal relationship between B1R expression after Ang II stimulation, suggesting a possible cross talk between AT1R and B1R in neuroinflammation and oxidative stress.
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