ReviewBritish journal of pharmacology2003
Bradykinin B2 receptor antagonism: a new direction for acute stroke therapy?
Review in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
9 citing papers in PubMed, 28 citations in OpenAlex.
- Role of uroguanylin's signalling pathway in the development of ischaemic stroke.The European journal of neuroscience · 2022Article
- Redox Regulation of Microvascular Permeability: IL-1β Potentiation of Bradykinin-Induced Permeability Is Prevented by Simvastatin.Antioxidants (Basel, Switzerland) · 2020Article
- Peptidase neurolysin functions to preserve the brain after ischemic stroke in male mice.Journal of neurochemistry · 2020Article
- Peptidase neurolysin is an endogenous cerebroprotective mechanism in acute neurodegenerative disorders.Medical hypotheses · 2019Article
- Impact of Bradykinin Generation During Thrombolysis in Ischemic Stroke.Frontiers in medicine · 2018Review
- Omapatrilat: penetration across the blood-brain barrier and effects on ischaemic stroke in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2015Article
- Involvement of bradykinin in brain edema development after ischemic stroke.Pflugers Archiv : European journal of physiology · 2015Review
- Acute NADPH oxidase activation potentiates cerebrovascular permeability response to bradykinin in ischemia-reperfusion.Free radical biology & medicine · 2011Article
- Effects of bradykinin postconditioning on endogenous antioxidant enzyme activity after transient forebrain ischemia in rat.Neurochemical research · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stroke is responsible for 10% of all deaths worldwide, and there remains an urgent need for the development of clinically effective treatments for acute stroke. Stroke is now considered to be a disease characterized by an ongoing inflammatory process rather than simply acute neurodegeneration. Bradykinin has attracted recent interest as a potential mediator of brain injury following stroke, because it activates several mechanisms responsible for the early manifestations of inflammation, including arteriolar dilatation, increased vascular permeability and oedema formation. These actions of bradykinin occur via activation of B(2) receptors. New evidence suggests that blocking bradykinin B(2) receptors after experimental cerebral ischaemia reduces brain oedema, infarct volume and neuronal necrosis, and improves neurological outcome. Thus, B(2) receptor antagonists may be a promising new class of compounds for clinical use after the onset of cerebral ischaemia.
Indexed as
Identifiers
What OpenQuestion holds
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.