Baroreflex activation in conscious rats modulates the joint inflammatory response via sympathetic function

Bassi, Gabriel Shimizu; Brognara, Fernanda; Castania, Jaci Airton; Talbot, Jhimmy; Cunha, Thiago Mattar; Cunha, Fernando de Queiróz; Ulloa, Luis; Kanashiro, Alexandre; Dias, Daniel Penteado Martins; Salgado, Hélio César

doi:10.1016/j.bbi.2015.05.002

Cited by 35 publications

(53 citation statements)

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“…We recently reported that baroreflex activation through electrical stimulation of the aortic depressor nerve (ADN) attenuates, via sympathetic innervation, joint inflammation in a rat model of arthritis. Our results depicted the baroreflex antiinflammatory pathway as a new physiological mechanism of neuromodulation of inflammation and the innate immune system (Bassi et al, 2015). …”

Section: Introductionmentioning

confidence: 74%

“…We recently reported that baroreflex activation attenuates local inflammation in arthritic knee joints (Bassi et al, 2015). This mechanism significantly inhibits neutrophil recruitment, articular edema and inflammatory cytokine levels in the synovial fluid (Bassi et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…This mechanism significantly inhibits neutrophil recruitment, articular edema and inflammatory cytokine levels in the synovial fluid (Bassi et al, 2015). This anti-inflammatory mechanism involves sympathetic modulation (Bassi et al, 2015); however, it is unknown whether baroreflex activation can control systemic inflammation. To expand knowledge about the anti-inflammatory potential of electrical stimulation of the baroreflex, we analyze, in the present study, whether baroreflex activation by electrical ADN stimulation controls systemic inflammation in endotoxemic rats.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2018

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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.

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Section: Introductionmentioning

confidence: 74%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

et al. 2018

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“…38 In conscious rats, loss of baroreflex function impedes attenuation of peripheral ( joint) inflammation, mediated by sympathetic neural drive. 39 Thus, acute inflammation superimposed on a lack of established baroreflex 'reserve' may further detrimentally impair the neural anti-inflammatory armamentarium, which consequently jeopardizes metabolic homeostasis. 40 We found that established baroreflex dysfunction was associated with a higher incidence of intraoperative blood transfusion.…”

Section: Discussionmentioning

confidence: 99%

Baroreflex impairment and morbidity after major surgery

Toner

Jenkins

Ackland

2016

British Journal of Anaesthesia

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Background: Baroreflex dysfunction is a common feature of established cardiometabolic diseases that are most frequently associated with the development of critical illness. Laboratory models show that baroreflex dysfunction impairs cardiac contractility and cardiovascular performance, thereby increasing the risk of morbidity after trauma and sepsis. We hypothesized that baroreflex dysfunction contributes to excess postoperative morbidity after major surgery as a consequence of the inability to achieve adequate perioperative tissue oxygen delivery. Methods: In a randomized controlled trial of goal-directed haemodynamic therapy (GDT) in higher-risk surgical patients, baroreflex function was assessed using the spontaneous baroreflex sensitivity (BRS) method via an arterial line placed before surgery, using a validated sequence method technique (one beat lag). The BRS was calculated during the 6 h postoperative GDT intervention. Analyses of BRS were done by investigators blinded to clinical outcomes. The primary outcome was the association between postoperative baroreflex dysfunction (BRS <6 mm Hg s −1 , a negative prognostic threshold in cardiovascular

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Spinal GABA-B receptor modulates neutrophil recruitment to the knee joint in zymosan-induced arthritis

Bassi

Malvar

Cunha

et al. 2016

Naunyn-Schmiedeberg's Arch Pharmacol

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Recent studies have demonstrated that the central nervous system controls inflammatory responses by activating complex efferent neuroimmune pathways. The present study was designed to evaluate the role that central gamma-aminobutyric acid type B (GABA-B) receptor plays in neutrophil migration in a murine model of zymosan-induced arthritis by using different pharmacological tools. We observed that intrathecal administration of baclofen, a selective GABA-B agonist, exacerbated the inflammatory response in the knee after zymosan administration characterized by an increase in the neutrophil recruitment and knee joint edema, whereas saclofen, a GABA-B antagonist, exerted the opposite effect. Intrathecal pretreatment of the animals with SB203580 (an inhibitor of p38 mitogen-activated protein kinase) blocked the pro-inflammatory effect of baclofen. On the other hand, systemic administration of guanethidine, a sympatholytic drug that inhibits catecholamine release, and nadolol, a beta-adrenergic receptor antagonist, reversed the effect of saclofen. Moreover, saclofen suppressed the release of the pro-inflammatory cytokines into the knee joint (ELISA) and pain-related behaviors (open field test). Since the anti-inflammatory effect of saclofen depends on the sympathetic nervous system integrity, we observed that isoproterenol, a beta-adrenergic receptor agonist, mimics the central GABA-B blockade decreasing knee joint neutrophil recruitment. Together, these results demonstrate that the pharmacological manipulation of spinal GABAergic transmission aids control of neutrophil migration to the inflamed joint by modulating the activation of the knee joint-innervating sympathetic terminal fibers through a mechanism dependent on peripheral beta-adrenergic receptors and central components, such as p38 MAPK.

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Baroreflex activation in conscious rats modulates the joint inflammatory response via sympathetic function

Cited by 35 publications

References 50 publications

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

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

Baroreflex impairment and morbidity after major surgery

Spinal GABA-B receptor modulates neutrophil recruitment to the knee joint in zymosan-induced arthritis

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