The involvement of hydroxyl radical and cyclooxygenase metabolites in the activation of lung vagal sensory receptors by circulatory endotoxin in rats

Lai, Chiung Ru; Ruan, Ting; Kou, Yu Ru

doi:10.1152/japplphysiol.00539.2004

Cited by 23 publications

(16 citation statements)

References 47 publications

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“…Only afferent fibers that showed stimulation within 2 s after the injection were studied. The conduction velocities of the VLCFs identified by this method have been shown to be within the range of C fibers [33], [34]. The general locations of all fibers were identified by their responses to the gentle pressing of the lungs with a saline-wetted cotton Q-tip.…”

Section: Methodsmentioning

confidence: 96%

Sensitization by Pulmonary Reactive Oxygen Species of Rat Vagal Lung C-Fibers: The Roles of the TRPV1, TRPA1, and P2X Receptors

Ruan

Lin²,

Hsu³

et al. 2014

PLoS ONE

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Sensitization of vagal lung C-fibers (VLCFs) induced by mediators contributes to the pathogenesis of airway hypersensitivity, which is characterized by exaggerated sensory and reflex responses to stimulants. Reactive oxygen species (ROS) are mediators produced during airway inflammation. However, the role of ROS in VLCF-mediated airway hypersensitivity has remained elusive. Here, we report that inhalation of aerosolized 0.05% H2O2 for 90 s potentiated apneic responses to intravenous capsaicin (a TRPV1 receptor agonist), α,β-methylene-ATP (a P2X receptor agonist), and phenylbiguanide (a 5-HT3 receptor agonist) in anesthetized rats. The apneic responses to these three stimulants were abolished by vagatomy or by perivagal capsaicin treatment, a procedure that blocks the neural conduction of VLCFs. The potentiating effect of H2O2 on the apneic responses to these VLCF stimulants was prevented by catalase (an enzyme that degrades H2O2) and by dimethylthiourea (a hydroxyl radical scavenger). The potentiating effect of H2O2 on the apneic responses to capsaicin was attenuated by HC-030031 (a TRPA1 receptor antagonist) and by iso-pyridoxalphosphate-6-azophenyl-2′,5′-disulphonate (a P2X receptor antagonist). The potentiating effect of H2O2 on the apneic responses to α,β-methylene-ATP was reduced by capsazepine (a TRPV1 receptor antagonist), and by HC-030031. The potentiating effect of H2O2 on the apneic responses to phenylbiguanide was totally abolished when all three antagonists were combined. Consistently, our electrophysiological studies revealed that airway delivery of aerosolized 0.05% H2O2 for 90 s potentiated the VLCF responses to intravenous capsaicin, α,β-methylene-ATP, and phenylbiguanide. The potentiating effect of H2O2 on the VLCF responses to phenylbiguanide was totally prevented when all antagonists were combined. Inhalation of 0.05% H2O2 indeed increased the level of ROS in the lungs. These results suggest that 1) increased lung ROS sensitizes VLCFs, which leads to exaggerated reflex responses in rats and 2) the TRPV1, TRPA1, and P2X receptors are all involved in the development of this airway hypersensitivity.

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Section: Methodsmentioning

confidence: 96%

Sensitization by Pulmonary Reactive Oxygen Species of Rat Vagal Lung C-Fibers: The Roles of the TRPV1, TRPA1, and P2X Receptors

Ruan

Lin²,

Hsu³

et al. 2014

PLoS ONE

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“…C-nerve fiber activation often coincides with RAR activation [46], as the two sensory receptors have been shown to respond to similar irritants. RARs are myelinated fibers located in the larynx, trachea, and bronchi [47].…”

Section: Airway Receptorsmentioning

confidence: 99%

Role of Autonomic Reflex Arcs in Cardiovascular Responses to Air Pollution Exposure

2014

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The body responds to environmental stressors by triggering autonomic reflexes in the pulmonary receptors, baroreceptors, and chemoreceptors to maintain homeostasis. Numerous studies have shown that exposure to various gases and airborne particles can alter the functional outcome of these reflexes, particularly with respect to the cardiovascular system. Modulation of autonomic neural input to the heart and vasculature following direct activation of sensory nerves in the respiratory system, elicitation of oxidative stress and inflammation, or through other mechanisms is one of the primary ways that exposure to air pollution affects normal cardiovascular function. Any homeostatic process that utilizes the autonomic nervous system to regulate organ function might be affected. Thus, air pollution and other inhaled environmental irritants have the potential to alter both local airway function and baro-and chemoreflex responses, which modulate autonomic control of blood pressure and detect concentrations of key gases in the body. While each of these reflex pathways causes distinct responses, the systems are heavily integrated and communicate through overlapping regions of the brainstem to cause global effects. This short review summarizes the function of major pulmonary sensory receptors, baroreceptors, and carotid body chemoreceptors and discusses the impacts of air pollution exposure on these systems.

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“…Endotoxin (Lai et al 2005) and reactive oxygen species (Ruan et al 2005) activate lung C fibers, which alter breathing frequency. Further, studies in humans identified a decrease in variability of respiratory timing with endotoxemia supporting an impact of systemic inflammation on breath-to-breath dynamics (Preas et al 2001).…”

Section: Introductionmentioning

confidence: 99%

Lung and brainstem cytokine levels are associated with breathing pattern changes in a rodent model of acute lung injury

Jacono¹,

Mayer²,

Hsieh³

et al. 2011

Respiratory Physiology & Neurobiology

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Acute lung injury evokes a pulmonary inflammatory response and changes in the breathing pattern. The inflammatory response has a centrally mediated component which depends on the vagi. We hypothesize that the central inflammatory response, complimentary to the pulmonary inflammatory response, is expressed in the nuclei tractus solitarii (nTS) and that the expression of cytokines in the nTS is associated with breathing pattern changes. Adult, male Sprague-Dawley rats (n=12) received intratracheal instillation of either bleomycin (3U in 120 µl of saline) or saline (120 µl). Respiratory pattern changed by 24h. At 48 h, bronchoalveolar lavage fluid and lung tissue had increased IL-1β and TNF-α levels, but not IL-6. No changes in these cytokines were noted in serum. Immunocytochemical analysis of the brainstem indicated increased expression of IL-1β in the nTS commissural subnucleus that was localized to neurons. We conclude that breathing pattern changes in acute lung injury were associated with increased levels of IL-1β in brainstem, areas which integrate cardio-respiratory sensory input.

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The involvement of hydroxyl radical and cyclooxygenase metabolites in the activation of lung vagal sensory receptors by circulatory endotoxin in rats

Cited by 23 publications

References 47 publications

Sensitization by Pulmonary Reactive Oxygen Species of Rat Vagal Lung C-Fibers: The Roles of the TRPV1, TRPA1, and P2X Receptors

Sensitization by Pulmonary Reactive Oxygen Species of Rat Vagal Lung C-Fibers: The Roles of the TRPV1, TRPA1, and P2X Receptors

Role of Autonomic Reflex Arcs in Cardiovascular Responses to Air Pollution Exposure

Lung and brainstem cytokine levels are associated with breathing pattern changes in a rodent model of acute lung injury

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