ArticlePflugers Archiv : European journal of physiology2006
Bradykinin shifts endothelial fluid passage from para- to transcellular routes.
Article in Pflugers Archiv : European journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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.
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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.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- The Bradykinin B2 Receptor Agonist (NG291) Causes Rapid Onset of Transient Blood-Brain Barrier Disruption Without Evidence of Early Brain Injury.Frontiers in neuroscience · 2021Article
- miR-200b restrains EMT and aggressiveness and regulates matrix composition depending on ER status and signaling in mammary cancer.Matrix biology plus · 2020Article
- Impedance analysis of GPCR-mediated changes in endothelial barrier function: overview and fundamental considerations for stable and reproducible measurements.Pflugers Archiv : European journal of physiology · 2015Article
- Article
- Endothelial cell permeability during hantavirus infection involves factor XII-dependent increased activation of the kallikrein-kinin system.PLoS pathogens · 2013Article
- Regulation of human organic anion transporter 3 by peptide hormone bradykinin.The Journal of pharmacology and experimental therapeutics · 2010Article
- Surface Plasmon Resonance Monitoring of Cell Monolayer Integrity: Implication of Signaling Pathways Involved in Actin-Driven Morphological Remodeling.Cellular and molecular bioengineering · 2008Article
- How steroid hormones act on the endothelium--insights by atomic force microscopy.Pflugers Archiv : European journal of physiology · 2008Review
- Nano-surgery at the leukocyte-endothelial docking site.Pflugers Archiv : European journal of physiology · 2008Article
- Bradykinin does not induce gap formation between human endothelial cells.Pflugers Archiv : European journal of physiology · 2008Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The signalling peptide bradykinin (BK) is implicated in inflammation and angiogenesis. It promotes fluid transport from blood vessels to interstitial space, and thus facilitates oedema formation. To clarify whether paracellular or transcellular pathways mediate this effect, we investigated the BK-stimulated fluid transport across endothelial monolayers in vitro by comparison of electrical and fluorescence methods. Electrical cell impedance sensing monitored a biphasic response of cell layers to BK with high time resolution: a short decrease (18%, 1 min) was followed by a more sustained increase in paracellular resistance (30%, 10 min). The two phases can be assigned to second messengers of the BK-signalling pathway: Ca(2+) for the decrease and cyclic adenosine monophosphate for the rise of resistance, respectively. Despite tightening of the intercellular clefts, BK increased the fluid permeability by 39%, indicating transcellular fluid transport. Additionally, BK stimulated both in- and outwardly directed membrane trafficking as assessed by vesicular fluid uptake (by 49%) and secretion of von Willebrandt factor (by 85%). In conclusion, the combination of electrical and fluorescence data suggests that BK induces a shift from para- to transcellular fluid transport across endothelium.
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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.