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Dihydrotestosterone stimulates cerebrovascular inflammation through NFkappaB, modulating contractile function.

Rayna J Gonzales1, Sue P Duckles, Diana N Krause

  • 1Department of Basic Sciences, University of Arizona College of Medicine-Phoenix, Phoenix, Arizona 85004, USA. rjgonzal@arizona.edu

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Dihydrotestosterone (DHT) activates the nuclear factor-kappaB (NFkappaB) pathway in cerebral blood vessels, increasing inflammation. This androgenic effect on the NFkappaB-COX-2/iNOS pathway may explain sex differences in cerebrovascular diseases.

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Area of Science:

  • Neuroscience
  • Cardiovascular Biology
  • Endocrinology

Background:

  • Testosterone's effects on cerebral circulation are complex, involving both androgenic and estrogenic actions.
  • Previous studies indicated testosterone augments vascular tone and exacerbates inflammation in the brain's blood vessels.

Purpose of the Study:

  • To investigate the impact of dihydrotestosterone (DHT), a non-aromatizable androgen, on the nuclear factor-kappaB (NFkappaB) inflammatory pathway in cerebral blood vessels.
  • To determine if DHT induces vascular inflammation via the NFkappaB pathway.

Main Methods:

  • Cerebral arteries were isolated from orchiectomized male rats.
  • Arteries were treated with DHT in vivo or ex vivo.
  • NFkappaB activation, cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) levels were measured.
  • Functional consequences were assessed using selective COX-2 and iNOS inhibitors.

Main Results:

  • DHT treatment increased nuclear NFkappaB activation in cerebral arteries.
  • DHT elevated levels of proinflammatory mediators COX-2 and iNOS.
  • These effects were partially blocked by flutamide, an androgen receptor antagonist.
  • Constriction responses to COX-2 and iNOS inhibitors were enhanced in DHT-treated arteries.

Conclusions:

  • The selective androgen receptor agonist DHT activates the NFkappaB pathway in cerebral blood vessels.
  • DHT promotes vascular inflammation by upregulating COX-2 and iNOS.
  • This DHT-induced inflammatory pathway may contribute to sex-based differences in cerebrovascular conditions.