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Angiotensin II induced cerebral microvascular inflammation and increased blood-brain barrier permeability via

M Zhang1, Y Mao, S H Ramirez

  • 1Department of Physiology, Temple University School of Medicine, Philadelphia, PA, USA.

Neuroscience
|September 28, 2010
PubMed

Insights

Hypertension mediated by angiotensin II (AngII) increases brain inflammation and blood-brain barrier permeability via oxidative stress. Antioxidant treatment attenuated these effects, suggesting new therapeutic targets for neurological conditions.

Area of Science:

  • Neuroscience
  • Cardiovascular Science
  • Immunology

Background:

  • Hypertension is linked to vascular disease, but its role in brain inflammation is not fully understood.
  • Angiotensin II (AngII) is a key mediator in hypertension and vascular responses.

Purpose of the Study:

  • To investigate the mechanisms by which AngII induces cerebral microvascular inflammation.
  • To determine the role of oxidative stress in AngII-mediated neuroinflammation and blood-brain barrier (BBB) disruption.

Main Methods:

  • Angiotensin II (AngII) infusion in C57BL/6 male mice to induce hypertension.
  • Intravital microscopy to assess leukocyte-endothelial interactions in pial vessels.
  • Evans Blue extravasation to measure blood-brain barrier (BBB) permeability.
  • Administration of the superoxide scavenger 4-hydroxy-TEMPO (Tempol) to evaluate its protective effects.

Main Results:

  • AngII infusion significantly increased leukocyte adhesion in cerebral microvasculature.
  • AngII infusion markedly elevated blood-brain barrier (BBB) permeability.
  • Treatment with Tempol attenuated leukocyte adhesion and protected BBB integrity.
  • Oxidative stress was identified as a key mediator in AngII-induced neuroinflammation.

Conclusions:

  • Angiotensin II (AngII) exacerbates cerebral microvascular inflammation and BBB permeability through oxidative stress.
  • Targeting oxidative stress may offer a therapeutic strategy for neurological disorders involving cerebrovascular inflammation.

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