Baroreflex stimulation attenuates central but not peripheral inflammation in conscious endotoxemic rats.

Journal Article (Journal Article)

We previously reported that activation of the baroreflex, a critical physiological mechanism controlling cardiovascular homeostasis, through electrical stimulation of the aortic depressor nerve attenuates joint inflammation in experimental arthritis. However, it is unknown whether baroreflex activation can control systemic inflammation. Here, we investigate whether baroreflex activation controls systemic inflammation in conscious endotoxemic rats. Animals underwent sham or electrical aortic depressor nerve stimulation initiated 10 min prior to a lipopolysaccharide (LPS) challenge, while inflammatory cytokine levels were measured in the blood, spleen, heart and hypothalamus 90 min after LPS treatment. Baroreflex activation did not affect LPS-induced levels of pro-inflammatory (tumor necrosis factor, interleukin 1β and interleukin 6) or anti-inflammatory (interleukin 10) cytokines in the periphery (heart, spleen and blood). However, baroreflex stimulation attenuated LPS-induced levels of all these cytokines in the hypothalamus. Notably, these results indicate that the central anti-inflammatory mechanism induced by baroreflex stimulation is independent of cardiovascular alterations, since aortic depressor nerve stimulation that failed to induce hemodynamic changes was also efficient at inhibiting inflammatory cytokines in the hypothalamus. Thus, aortic depressor nerve stimulation might represent a novel therapeutic strategy for neuroprotection, modulating inflammation in the central nervous system.

Full Text

Duke Authors

Cited Authors

  • Brognara, F; Castania, JA; Dias, DPM; Lopes, AH; Fazan, R; Kanashiro, A; Ulloa, L; Salgado, HC

Published Date

  • March 1, 2018

Published In

Volume / Issue

  • 1682 /

Start / End Page

  • 54 - 60

PubMed ID

  • 29317289

Pubmed Central ID

  • PMC6262230

Electronic International Standard Serial Number (EISSN)

  • 1872-6240

Digital Object Identifier (DOI)

  • 10.1016/j.brainres.2018.01.003


  • eng

Conference Location

  • Netherlands