Physiological Sympathetic Activation Reduces Systemic Inflammation: Role of Baroreflex and Chemoreflex

Abstract

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)-1β; (III) increased the plasma levels of anti-inflammatory cytokine IL-10, 90 min after LPS administration. Moreover, selective baroreceptor or chemoreceptor denervation deactivated mechanosensitive and chemical sensors, respectively, and decreased the release of the LPS-induced cytokine but did not alter the BCO modulatory effects. These results show, for the first time, that physiological reflex activation of the sympathetic circuit decreases the inflammatory response in endotoxemic rats and suggest a novel function for the baroreceptors as immunosensors during the systemic inflammation.

Similar Patterns of Dysautonomia in Myalgic Encephalomyelitis/Chronic Fatigue and Post-COVID-19 Syndromes

“…Several potential mechanisms connecting an abnormal baroreflex to fatigue and cognitive impairment has been suggested, including reduced or dysregulated cerebral perfusion, the effects of decreased vagal afferent inputs to the nucleus tractus solitarii on higher cortical networks [ 30 ], and deactivation of the physiological baroreflex-induced reduction in systemic inflammation and neuroinflammation [ 32 , 33 ]. Therefore, baroreflex dysfunction possibly contributes to the reduction in cerebral blood flow, which has been reported in ME/CFS and PCC [ 5 ].…”

Does fetal growth restriction induce neuropathology within the developing brainstem?

“…The NTS plays a principal role in processing and coordinating hypoxia‐induced respiratory and sympathetic and parasympathetic responses, and is the first synaptic relay of afferent inputs from the chemo‐ and baroreceptors (Brognara et al., 2021 ; Zoccal et al., 2014 ). The NTS pathways to the NA and DMNV convey a variety of signals, including those arising from arterial baro‐ and chemo‐receptors, and from cardiopulmonary receptors that alter cardiovagal nerve activity (McAllen & Spyer, 1978 ).…”

Autonomic Regulation of Inflammation in Conscious Animals

“…Therefore, BCO, a physiological approach involving baroreflex and chemoreflex mechanisms, associated with the baroreceptors and peripheral chemoreceptors from the cardiovascular system, was applied for 20s to conscious rats [79]. Our results showed for the first time that a physiological reflex activation of the sympathetic circuit using BCO decreases the systemic inflammatory responses in endotoxemic rats, and also suggest that the higher the sympathetic modulation of the resistance vessels during the BCO, the lower the pro-inflammatory cytokine release induced by LPS; a negative correlation was found between the sympathetic modulation and cytokine production [79].…”