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- W2432167425 abstract "Although angiotensin II (Ang II) has been shown to cause endothelial dysfunction, its role in inflammatory responses, especially in brain, remains unclear. The goal of this study is to investigate the mechanisms through which Ang II mediates cerebral microvascular inflammation. C57BL/6 male mice were subjected to slow pressor dose of Ang II infusion (Alzet mini-pump) ata rate of 400ng/kg/min for 14 days. Intravital microscopic observation was used to investigate the leukocyte/endothelial interactions in pial microvessels in vivo. A superoxide scavenger 4-hydroxy-TEMPO (Tempol) was added to drinking water (2mmol) on day 4th following Ang II infusion. Blood-brain barrier (BBB) permeability was evaluated by Evans Blue extravasation ex vivo. Ang II increased (p<0.01) the leukocyte adhesion on day 4th of infusion compared to vehicle. This effect was maintained on day 14th (p<0.05) and also was accompanied with an increase of leukocyte rolling (p<0.01). Ang II increased the BBB permeability on day 14th (p<0.05). Tempol attenuated the increased leukocyte/endothelial interactions and protected the BBB integrity (p<0.01). In conclusion, Ang II causes cerebral microvasculature inflammation, which leads to the increased BBB permeability. This effect of Ang II is, at least in part mediated via oxidative stress since Tempol reverses the leukocyte rolling and adhesion, and prevents the increased BBB permeability." @default.
- W2432167425 created "2016-06-24" @default.
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- W2432167425 date "2010-04-01" @default.
- W2432167425 modified "2023-10-17" @default.
- W2432167425 title "Angiotensin II Induced Cerebral Microvascular Inflammation and Increased Blood‐Brain Barrier Permeability via Oxidative Stress" @default.
- W2432167425 doi "https://doi.org/10.1096/fasebj.24.1_supplement.590.1" @default.
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