ArticlePloS one2012
Deficient dopamine D2 receptor function causes renal inflammation independently of high blood pressure.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 49 citations in OpenAlex.
- Differential methylation in blood pressure control genes is associated to essential hypertension in African Brazilian populations.Epigenetics · 2025Article
- Animal models of hypertension and concurrent organs injury.Animal models and experimental medicine · 2025Review
- Dopamine receptors and organ fibrosis.Biochemistry and biophysics reports · 2025Review
- Comprehensive Analysis of Multi-Omics Data on RNA Polymerase as an Adverse Factor in Head and Neck Squamous Cell Carcinoma.Journal of inflammation research · 2025Article
- An Overview on Renal and Central Regulation of Blood Pressure by Neuropeptide FF and Its Receptors.International journal of molecular sciences · 2024Review
- Anti-Inflammatory Effects of Peripheral Dopamine.International journal of molecular sciences · 2023Review
- Correlation between the dopaminergic system and inflammation disease: a review.Molecular biology reports · 2023Review
- Inverse Salt Sensitivity of Blood Pressure Is Associated with an Increased Renin-Angiotensin System Activity.Biomedicines · 2022Article
- Inverse Salt Sensitivity of Blood Pressure: Mechanisms and Potential Relevance for Prevention of Cardiovascular Disease.Current hypertension reports · 2022Review
- Role of protein phosphatase 2A in kidney disease (Review).Experimental and therapeutic medicine · 2021Review
- Renal Dopamine Receptors and Oxidative Stress: Role in Hypertension.Antioxidants & redox signaling · 2021Review
- Dopamine Receptors and the Kidney: An Overview of Health- and Pharmacological-Targeted Implications.Biomolecules · 2021Review
- The Role of the Renal Dopaminergic System and Oxidative Stress in the Pathogenesis of Hypertension.Biomedicines · 2021Review
- Involvement of dopaminergic signaling in the cross talk between the renin-angiotensin system and inflammation.Seminars in immunopathology · 2020Review
- Dopamine activates NF-κB and primes the NLRP3 inflammasome in primary human macrophages.Brain, behavior, & immunity - health · 2020Article
- Dopamine DScientific reports · 2019Article
- Genetic polymorphisms associated with reactive oxygen species and blood pressure regulation.The pharmacogenomics journal · 2019Review
- Role of Macrophage Dopamine Receptors in Mediating Cytokine Production: Implications for Neuroinflammation in the Context of HIV-Associated Neurocognitive Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019Article
- G protein-coupled receptor 37L1 regulates renal sodium transport and blood pressure.American journal of physiology. Renal physiology · 2019Article
- Dopamine D2 receptor restricts astrocytic NLRP3 inflammasome activation via enhancing the interaction of β-arrestin2 and NLRP3.Cell death and differentiation · 2018Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Renal dopamine receptors participate in the regulation of blood pressure. Genetic factors, including polymorphisms of the dopamine D(2) receptor gene (DRD2) are associated with essential hypertension, but the mechanisms of their contribution are incompletely understood. Mice lacking Drd2 (D(2)-/-) have elevated blood pressure, increased renal expression of inflammatory factors, and renal injury. We tested the hypothesis that decreased dopamine D(2) receptor (D(2)R) function increases vulnerability to renal inflammation independently of blood pressure, is an immediate cause of renal injury, and contributes to the subsequent development of hypertension. In D(2)-/- mice, treatment with apocynin normalized blood pressure and decreased oxidative stress, but did not affect the expression of inflammatory factors. In mouse RPTCs Drd2 silencing increased the expression of TNFα and MCP-1, while treatment with a D(2)R agonist abolished the angiotensin II-induced increase in TNF-α and MCP-1. In uni-nephrectomized wild-type mice, selective Drd2 silencing by subcapsular infusion of Drd2 siRNA into the remaining kidney produced the same increase in renal cytokines/chemokines that occurs after Drd2 deletion, increased the expression of markers of renal injury, and increased blood pressure. Moreover, in mice with two intact kidneys, short-term Drd2 silencing in one kidney, leaving the other kidney undisturbed, induced inflammatory factors and markers of renal injury in the treated kidney without increasing blood pressure. Our results demonstrate that the impact of decreased D(2)R function on renal inflammation is a primary effect, not necessarily associated with enhanced oxidant activity, or blood pressure; renal damage is the cause, not the result, of hypertension. Deficient renal D(2)R function may be of clinical relevance since common polymorphisms of the human DRD2 gene result in decreased D(2)R expression and function.
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Registered trials
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