Physiological Sympathetic Activation Reduces Systemic Inflammation: Role of Baroreflex and Chemoreflex.
Animals
Autonomic Nervous System
/ physiology
Baroreflex
/ physiology
Blood Pressure
/ physiology
Chemoreceptor Cells
/ physiology
Endotoxemia
/ pathology
Inflammation
/ physiopathology
Interleukin-10
/ blood
Interleukin-1beta
/ blood
Lipopolysaccharides
Pressoreceptors
/ physiology
Rats
Rats, Wistar
Sympathetic Nervous System
/ physiology
Tumor Necrosis Factor-alpha
/ blood
baroreceptors
bilateral carotid occlusion
chemoreceptors
inflammation
neuroimmune interactions
sympathetic activation
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2021
2021
Historique:
received:
04
12
2020
accepted:
06
04
2021
entrez:
17
5
2021
pubmed:
18
5
2021
medline:
24
9
2021
Statut:
epublish
Résumé
Baroreflex and chemoreflex act through the autonomic nervous system, which is involved with the neural regulation of inflammation. The present study reports the effects of reflex physiological sympathetic activation in endotoxemic rats using bilateral carotid occlusion (BCO), a physiological approach involving the baroreflex and chemoreflex mechanisms and the influence of the baroreceptors and peripheral chemoreceptors in the cardiovascular and systemic inflammatory responses. After lipopolysaccharide (LPS) administration, the arterial pressure was recorded during 360 min in unanesthetized rats, and serial blood samples were collected to analyze the plasma cytokine levels. BCO elicited the reflex activation of the sympathetic nervous system, providing the following outcomes: (I) increased the power of the low-frequency band in the spectrum of the systolic arterial pressure during the BCO period; (II) reduced the levels of pro-inflammatory cytokines in plasma, including the tumor necrosis factor (TNF) and the interleukin (IL)-1
Identifiants
pubmed: 33995355
doi: 10.3389/fimmu.2021.637845
pmc: PMC8117744
doi:
Substances chimiques
IL1B protein, rat
0
Interleukin-1beta
0
Lipopolysaccharides
0
Tumor Necrosis Factor-alpha
0
Interleukin-10
130068-27-8
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
637845Informations de copyright
Copyright © 2021 Brognara, Castania, Kanashiro, Dias and Salgado.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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