Sensitivity of vagal afferent endings to chemical irritants in the rat lung

Ho, Ching‐Yin; Gu, Qihai; Lin, Yun‐Sheng; Lee, L.-Y

doi:10.1016/s0034-5687(01)00241-9

Cited by 185 publications

(209 citation statements)

References 21 publications

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“…Similar to that reported previously (Ho et al, 2001), pulmonary C-fiber afferents usually have no or low baseline activity at control (e.g., Fig. 1).…”

Section: Study Seriessupporting

confidence: 88%

“…On the other hand, hyperthermia may also activate certain temperature sensitive ion channels, particularly the transient receptor potential vanilloid type (TRPV) channels. In fact, expression of the TRPV1 receptors on the sensory terminals has been considered one of the most distinct characteristic features of the pulmonary C-fiber afferents (Ho et al, 2001), although the temperature threshold for activating the TRPV1 (> 43°C) exceeds the physiological range of body temperature that was applied in our studies. To test this possibility, a follow-up study was recently carried out in isolated rat vagal pulmonary sensory neurons (Ni et al, 2006).…”

Section: Discussionmentioning

confidence: 84%

“…The conventional method for identifying and recording single-unit pulmonary C-fiber activity, as previously described (Ho et al, 2001), was used in this study. Briefly, the right cervical vagus nerve was separated from the carotid artery and sectioned rostrally.…”

Section: Recording Of Single-unit Pulmonary C-fiber Activitymentioning

confidence: 99%

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Prostaglandin E2 enhances the sensitizing effect of hyperthermia on pulmonary C-fibers in rats

Zhang

Lee

2007

Respiratory Physiology & Neurobiology

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This study was carried out to investigate whether the pulmonary C-fiber hypersensitivity induced by hyperthermia is altered by prostaglandin E 2 (PGE 2 ). Single-unit afferent activities of pulmonary C-fibers were recorded in anesthetized, artificially ventilated rats when the intrathoracic temperature (T it ) was maintained at normal (N; ~36°C) and hyperthermia levels (H; ~41°C) by perfusion of heated saline into the thoracic chamber for 3 min. After ~20 min of recovery, the fiber activities were recorded again during infusion of PGE 2 at both N and H levels of T it . Our study showed: 1) The baseline fiber activity and responses to lung inflation, right atrial injection of capsaicin and adenosine were all increased by increasing T it from N to H, and these hyperthermia-induced increases in sensitivities were also significantly augmented by PGE 2 . 2) These enhanced sensitivities induced by PGE 2 were abolished by pretreatment with AH6809 and AH23848, selective antagonists of EP 2 and EP 4 prostanoid receptors, respectively. In conclusion, the hyperthermia-induced hypersensitivity of vagal pulmonary C-fibers is potentiated by PGE 2 , and this effect is mediated through activation of EP 2 and EP 4 prostanoid receptors.

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“…Similar to that reported previously (Ho et al, 2001), pulmonary C-fiber afferents usually have no or low baseline activity at control (e.g., Fig. 1).…”

Section: Study Seriessupporting

confidence: 88%

Section: Discussionmentioning

confidence: 84%

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Prostaglandin E2 enhances the sensitizing effect of hyperthermia on pulmonary C-fibers in rats

Zhang

Lee

2007

Respiratory Physiology & Neurobiology

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“…In healthy lungs, TRPV1 is selectively expressed in smalldiameter, slow-conducting nonmyelinated (C-) fibers that represent a majority (Ͼ75%) of vagal afferents innervating the lung and airways (30,31), and TRPA1 is found to be coexpressed with TRPV1 in a subset of these vagal C-fiber afferent nerves (5,40). Both TRPV1 and TRPA1 are recognized as the primary transducers located in the bronchopulmonary C-fiber sensory terminals that can be activated by a wide range of endogenous inflammatory mediators and activators (e.g., protons, hyperthermia, bradykinin, reactive oxygen radicals, etc.)…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, this effect seems to involve specifically an upregulation of the sensitivity and/or expression of transient receptor potential vanilloid type 1 (TRPV1) induced by the TNF␣ pretreatment in DRG neurons; TRPV1 is a polymodal transducer and expressed predominantly in nonmyelinated (C-fiber) afferents (11,30). Bronchopulmonary C-fibers represent Ͼ75% of the vagal afferents innervating the lungs and airways and are the counterpart of the DRG nociceptive endings in the lung structures.…”

mentioning

confidence: 99%

Calcium transient evoked by TRPV1 activators is enhanced by tumor necrosis factor-α in rat pulmonary sensory neurons

Gu²,

Lin³

et al. 2010

American Journal of Physiology-Lung Cellular and Molecular Phys

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Hu Y, Gu Q, Lin RL, Kryscio R, Lee LY. Calcium transient evoked by TRPV1 activators is enhanced by tumor necrosis factor-␣ in rat pulmonary sensory neurons. Am J Physiol Lung Cell Mol Physiol 299: L483-L492, 2010. First published July 16, 2010 doi:10.1152/ajplung.00111.2010.-TNF␣, a proinflammatory cytokine known to be involved in the pathogenesis of allergic asthma, has been shown to induce hyperalgesia in somatic tissue via a sensitizing effect on dorsal root ganglion neurons expressing transient receptor potential vanilloid type 1 receptor (TRPV1). Because TRPV1-expressing pulmonary sensory neurons play an important role in regulating airway function, this study was carried out to determine whether TNF␣ alters the sensitivity of these neurons to chemical activators. Responses of isolated nodose and jugular ganglion neurons innervating the rat lungs were determined by measuring the transient increase in intracellular Ca 2ϩ concentration ([Ca 2ϩ ]i). Our results showed the following. 1) A pretreatment with TNF␣ (50 ng/ml) for ϳ24 h increased significantly the peak ⌬[Ca 2ϩ ]i evoked by capsaicin (Cap) in these neurons. A pretreatment with the same concentration of TNF␣ for a longer duration (ϳ48 h) did not further increase the response, but pretreatment for a shorter duration (1 h) or with a lower concentration (25 ng/ml, 24 h) failed to enhance the Cap sensitivity.2) The same TNF␣ pretreatment also induced similar but less pronounced and less uniform increases in the responses to acid (pH 6.5-5.5), 2-aminoethoxydiphenyl borate (2-APB), a common activator of TRPV1, V2, and V3 channels, and allyl isothiocyanate (AITC), a selective activator of TRPA1 channel. 3) In sharp contrast, the responses to ATP, ACh, and KCl were not affected by TNF␣. 4) The TNF␣-induced hypersensitivity to Cap was not prevented by pretreatment with indomethacin (30 M). 5) The immunoreactivity to both TNF receptor types 1 and 2 were detected in rat vagal pulmonary sensory neurons. In conclusion, prolonged treatment with TNF␣ induces a pronounced potentiating effect on the responses of isolated pulmonary sensory neurons to TRPV1 activators. This action of TNF␣ may contribute in part to the airway hyperresponsiveness induced by this cytokine. intracellular calcium; pulmonary afferent; transient receptor potential vanilloid type 1; airway inflammation; asthma AN IMPORTANT ROLE OF TNF␣ in the pathogenesis of allergic asthma has been extensively documented (6,9,28,47). TNF␣ can be released from a variety of cell types in the airways, particularly macrophages, monocytes, and mast cells. TNF␣, either newly synthesized or preformed and stored constitutively within the mast cell granules, is coreleased with other potent mediators such as histamine and tryptase via the IgE-dependent mechanism (9, 21, 47). TNF␣ was detected in bronchoalveolar lavage fluid, sputum, exhaled breath condensate, and serum of asthmatic patients during asthmatic attack or following antigen inhalation challenge (12,33,39). Furthermore, it has been shown that TNF␣ is releas...

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Cough: Causes, Mechanisms and Therapy

Chung¹,

Widdicombe²,

Boushey³

2003

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Sensitivity of vagal afferent endings to chemical irritants in the rat lung

Cited by 185 publications

References 21 publications

Prostaglandin E2 enhances the sensitizing effect of hyperthermia on pulmonary C-fibers in rats

Prostaglandin E2 enhances the sensitizing effect of hyperthermia on pulmonary C-fibers in rats

Calcium transient evoked by TRPV1 activators is enhanced by tumor necrosis factor-α in rat pulmonary sensory neurons

Cough: Causes, Mechanisms and Therapy

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