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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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Author(s):
Brognara, Fernanda [1] ; Castania, Jaci A. [1] ; Dias, Daniel P. M. [1] ; Lopes, Alexandre H. [2] ; Fazan, Jr., Rubens [1] ; Kanashiro, Alexandre [3] ; Ulloa, Luis [4] ; Salgado, Helio C. [1]
Total Authors: 8
Affiliation:
[1] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Physiol, Av Bandeirantes 3900, BR-14049900 Ribeirao Preto, SP - Brazil
[2] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Pharmacol, Ribeirao Preto, SP - Brazil
[3] Univ Fed Sao Carlos, Dept Physiol Sci, Sao Carlos, SP - Brazil
[4] Rutgers State Univ, Dept Surg, Ctr Immunol & Inflammat, New Jersey Med Sch, Newark, NJ 07103 - USA
Total Affiliations: 4
Document type: Journal article
Source: Brain Research; v. 1682, p. 54-60, MAR 1 2018.
Web of Science Citations: 4
Abstract

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 1 beta 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. (C) 2018 Elsevier B.V. All rights reserved. (AU)

FAPESP's process: 14/15386-4 - Modulation of the inflammatory response to LPS by electrical activation of the baroreflex in conscious rats
Grantee:Fernanda Brognara Penteado Dias
Support Opportunities: Scholarships in Brazil - Scientific Initiation
FAPESP's process: 11/20343-4 - Antiinflammatory cholinergic pathway: the role of neuroimmunomodulation in the control of inflammatory response
Grantee:Alexandre Kanashiro
Support Opportunities: Research Grants - Young Investigators Grants
FAPESP's process: 13/20549-7 - New insights in cardiovascular regulation under physiological and pathophysiological condition
Grantee:Helio Cesar Salgado
Support Opportunities: Research Projects - Thematic Grants
FAPESP's process: 17/05163-6 - Role of the parasympathetic and sympathetic autonomic nervous system in the modulation of sepsis in unanesthetized rats
Grantee:Fernanda Brognara Penteado Dias
Support Opportunities: Scholarships in Brazil - Doctorate (Direct)