ArticleBlood2008
Circulating neutrophils maintain physiological blood pressure by suppressing bacteria and IFNgamma-dependent iNOS expression in the vasculature of healthy mice.
Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 50 citations in OpenAlex.
- Meta-analysis of differences in neutrophil to lymphocyte ratio between hypertensive and non-hypertensive individuals.BMC cardiovascular disorders · 2023Pooled it
- A meta-analysis of gene expression signatures of blood pressure and hypertension.PLoS genetics · 2015Pooled it
- White Blood Cells and Blood Pressure: A Mendelian Randomization Study.Circulation · 2020Trial
- Pathophysiology and Clinical Relevance of Microvascular Remodeling in Arterial Hypertension.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2026Review
- Sheep erythrocyte potassium locus highlights MYADM family regulation of electroneutral potassium chloride cotransporters (KCC).BMC genomics · 2026Article
- Innate immunity and hypertension: unveiling inflammatory pathways for novel therapies.Frontiers in pharmacology · 2026Review
- Neutrophil Heterogeneity after Myocardial Infarction.Journal of innate immunity · 2026Review
- Role of Neutrophil Extracellular Traps in Hypertension and Their Impact on Target Organs.Journal of clinical hypertension (Greenwich, Conn.) · 2025Review
- The roles of neutrophils in cardiovascular diseases.Frontiers in cardiovascular medicine · 2025Review
- Immune and inflammatory mechanisms in hypertension.Nature reviews. Cardiology · 2024Review
- Mechanisms of inflammation modulation by different immune cells in hypertensive nephropathy.Frontiers in immunology · 2024Review
- Th1 Cells Alter the Inflammatory Signature of IL-6 by Channeling STAT Transcription Factors to Alu-like Retroelements.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Article
- Innate Immune Cells and Hypertension: Neutrophils and Neutrophil Extracellular Traps (NETs).Comprehensive Physiology · 2021Review
- The Role of Neutrophils in Hypertension.International journal of molecular sciences · 2020Review
- AT1R Activating Autoantibodies in Hematopoietic Stem Cell Transplantation.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2020Article
- Mouse Models and Tools for theFrontiers in immunology · 2019Review
- Novel Immune Mechanisms in Hypertension and Cardiovascular Risk.Current cardiovascular risk reports · 2017Review
- Genetic and Pharmacologic Inhibition of the Chemokine Receptor CXCR2 Prevents Experimental Hypertension and Vascular Dysfunction.Circulation · 2016Article
- Gut Microbiota Promote Angiotensin II-Induced Arterial Hypertension and Vascular Dysfunction.Journal of the American Heart Association · 2016Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
Abstract
Whether leukocytes exert an influence on vascular function in vivo is not known. Here, genetic and pharmacologic approaches show that the absence of neutrophils leads to acute blood pressure dysregulation. Following neutrophil depletion, systolic blood pressure falls significantly over 3 days (88.0 +/- 3.5 vs 104.0 +/- 2.8 mm Hg, day 3 vs day 0, mean +/- SEM, P < .001), and aortic rings from neutropenic mice do not constrict properly. The constriction defect is corrected using l-nitroarginine-methyl ester (L-NAME) or the specific inducible nitric oxide synthase (iNOS) inhibitor 1400W, while acetylcholine relaxation is normal. iNOS- or IFNgamma-deficient mice are protected from neutropenia-induced hypotension, indicating that iNOS-derived nitric oxide (NO) is responsible and that its induction involves IFNgamma. Oral enrofloxacin partially inhibited hypotension, implicating bacterial products. Roles for cyclooxygenase, complement C5, or endotoxin were excluded, although urinary prostacyclin metabolites were elevated. Neutrophil depletion required complement opsinization, with no evidence for intravascular degranulation. In summary, circulating neutrophils contribute to maintaining physiological tone in the vasculature, at least in part through suppressing early proinflammatory effects of infection. The speed with which hypotension developed provides insight into early changes that occur in the absence of neutrophils and illustrates the importance of constant surveillance of mucosal sites by granulocytes in healthy mice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.