ArticleFree radical biology & medicine2011
Acute NADPH oxidase activation potentiates cerebrovascular permeability response to bradykinin in ischemia-reperfusion.
Article in Free radical biology & medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Therapeutic Potential of PCSK9 Inhibitors in Regulating Neuroinflammation in Acute Ischemic Stroke.CNS drugs · 2026Review
- Normobaric Hyperoxia Therapy in Treating Stroke.Clinical interventions in aging · 2025Review
- Redox Regulation of Microvascular Permeability: IL-1β Potentiation of Bradykinin-Induced Permeability Is Prevented by Simvastatin.Antioxidants (Basel, Switzerland) · 2020Article
- Reactive oxygen species facilitate the EDH response in arterioles by potentiating intracellular endothelial Ca(2+) release.Free radical biology & medicine · 2016Article
- NOX Activation by Subunit Interaction and Underlying Mechanisms in Disease.Frontiers in cellular neuroscience · 2016Review
- Efficacy of prophylactic flavan-3-ol in permanent focal ischemia in 12-mo-old mice.American journal of physiology. Heart and circulatory physiology · 2015Article
- Temporal and spatial distribution of Nrf2 in rat brain following stroke: quantification of nuclear to cytoplasmic Nrf2 content using a novel immunohistochemical technique.The Journal of physiology · 2013Article
- Cardiac inflammation after local irradiation is influenced by the kallikrein-kinin system.Cancer research · 2012Article
- Targeting microglia-mediated neurotoxicity: the potential of NOX2 inhibitors.Cellular and molecular life sciences : CMLS · 2012Review
- NADPH oxidase in stroke and cerebrovascular disease.Neurological research · 2012Review
- Normobaric hyperoxia protects the blood brain barrier through inhibiting Nox2 containing NADPH oxidase in ischemic stroke.Medical gas research · 2011Article
- Implication of the Kallikrein-Kinin system in neurological disorders: Quest for potential biomarkers and mechanisms.Progress in neurobiologyReview
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5 authors at 1 institution in 1 country.
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Abstract
Free radical generation is a key event in cerebral reperfusion injury. Bradykinin (Bk) and interleukin-1β (IL-1β) have both been implicated in edema formation after stroke, although acute Bk application itself results in only a modest permeability increase. We have investigated the molecular mechanism by assessing the permeability of single pial venules in a stroke model. Increased permeability on reperfusion was dependent on the duration of ischemia and was prevented by applying the B(2) receptor antagonist HOE 140. Postreperfusion permeability increases were mimicked by applying Bk (5μM) for 10 min and blocked by coapplying the IL-1 receptor antagonist with Bk. Furthermore, 10 min pretreatment with IL-1β resulted in a 3 orders of magnitude leftward shift of the acutely applied Bk concentration-response curve. The left shift was abolished by scavenging free radicals with superoxide dismutase and catalase. Apocynin coapplied with IL-1β completely blocked the potentiation, implying that NADPH oxidase assembly is the immediate target of IL-1β. In conclusion, this is first demonstration that bradykinin, released during cerebral ischemia, leads to IL-1β release, which in turn activates NADPH oxidase leading to blood-brain barrier breakdown.
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