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Brain perivascular macrophages and the sympathetic response to inflammation in rats after myocardial infarction

Yang Yu1, Zhi-Hua Zhang, Shun-Guang Wei

  • 1Department of Veterans' Affairs Medical Center, Iowa City, Iowa, USA.

Hypertension (Dallas, Tex. : 1979)
|February 10, 2010
PubMed

Insights

Inflammation after heart attack increases sympathetic nerve activity via brain inflammation. Blocking specific brain cells reduced this effect, suggesting a new therapeutic target for cardiovascular diseases.

Area of Science:

  • Cardiovascular Physiology
  • Neuroinflammation
  • Sympathetic Nervous System Regulation

Background:

  • Inflammation is linked to increased sympathetic drive in cardiovascular diseases.
  • Proinflammatory cytokines can activate cyclooxygenase 2 (COX-2) in brain perivascular macrophages.
  • This activation may lead to prostaglandin E(2) production, increasing sympathetic nerve activity.

Purpose of the Study:

  • To investigate the role of brain perivascular macrophages and COX-2 in augmented sympathetic drive post-myocardial infarction (MI) in rats.

Main Methods:

  • Rats underwent myocardial infarction (MI) and received intracerebroventricular injections of clodronate liposomes to deplete perivascular macrophages.
  • COX-2 expression, prostaglandin E(2) levels, neuronal activity, and plasma norepinephrine were measured.
  • Responses to tumor necrosis factor-alpha were assessed in normal rats pretreated with clodronate liposomes.

Main Results:

  • MI increased COX-2 in hypothalamic paraventricular nucleus perivascular macrophages and prostaglandin E(2) levels.
  • Depleting perivascular macrophages (MI+CLOD) normalized COX-2 and reduced prostaglandin E(2), neuronal excitation, and plasma norepinephrine compared to MI rats.
  • Clodronate liposomes reduced sympathetic, blood pressure, and heart rate responses to tumor necrosis factor-alpha.

Conclusions:

  • Proinflammatory cytokines stimulate sympathetic excitation after MI by inducing COX-2 and prostaglandin E(2) in brain perivascular macrophages.
  • Targeting these perivascular macrophages may offer a novel therapeutic strategy for managing sympathetic overactivity in cardiovascular disease.

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