Afferent vagal C fibre innervation of the lungs and airways and its functional significance

Coleridge, J. C. G.; Coleridge, H. M.

doi:10.1007/bfb0027715

Cited by 607 publications

(590 citation statements)

References 205 publications

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“…Furthermore, activation of the pulmonary C-fiber afferents is known to elicit powerful and extensive systemic reflex responses such as rapid shallow breathing, bronchoconstriction, hypersecretion of mucus, cough, arterial hypotension, etc. (Coleridge and Coleridge, 1984;Lee and Pisarri, 2002). This synergistic effect may, therefore, play a part in the manifestation of airway hypersensitivity associated with airway inflammatory reactions.…”

Section: Discussionmentioning

confidence: 99%

“…These nonmyelinated pulmonary afferents are known to play an important role in protecting the lung under normal and pathophysiological conditions. Stimulation of these afferents can elicit extensive centrally-mediated reflex responses, including apnea, rapid shallow breathing, hypotension and bradycardia, bronchoconstriction, hypersecretion of mucus and cough (Coleridge and Coleridge, 1984;Lee and Pisarri, 2001).…”

Section: Introductionmentioning

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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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Zhang

Lee

2007

Respiratory Physiology & Neurobiology

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“…The short burst of EaTA, disappearing well before the end of the inspiratory pressure plateau in nPSV (see figure 3 in Moreau-Bussière et al, 2007), does not suggest the involvement of SAR. While both RARs and CFEs are also stimulated by lung distension (Coleridge JCG and Coleridge HM, 1984;Coleridge HM and Coleridge JCG, 2011), our previous observation that stimulation of pulmonary CFEs in lambs triggers post-inspiratory EaTA (Diaz et al, 1999), together with the availability of our robust lamb model with blocked CFEs, prompted us to assess the potential involvement of CFEs in inspiratory laryngeal narrowing during nPSV. The present demonstration that CEFs are not involved leads us now to suggest that this inspiratory laryngeal narrowing most likely originates from RAR stimulation.…”

Section: 1-inspiratory Laryngeal Narrowing During Npsvmentioning

confidence: 99%

“…The complex effects of lung inflation on these receptors have been summarized as follows (Coleridge JCG and Coleridge HM, 1984;Coleridge HM and Coleridge JCG, 2011). Slowly-adapting receptors are stimulated by moderate lung inflation and are involved in the inspiratory switch-off during normal breathing.…”

Section: Introductionmentioning

confidence: 99%

Laryngeal narrowing during nasal ventilation does not originate from bronchopulmonary C-fibers

Samson

Niane

Nault

et al. 2014

Respiratory Physiology & Neurobiology

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We previously showed that nasal pressure support ventilation (nPSV) can lead to active inspiratory laryngeal narrowing, which originates from the stimulation of bronchopulmonary receptors. Among the three major types of bronchopulmonary receptors, which are variably stimulated by lung distension, C-fiber endings are remarkable, given that their stimulation can also trigger laryngeal closure. Taking advantage of our lamb model with blocked C-fibers, we aimed to assess whether bronchopulmonary C-fiber endings are involved in the active inspiratory laryngeal narrowing during nPSV. Nine lambs were surgically instrumented to assess states of alertness, electrical activity of a glottal constrictor (EaTA), respiratory movements and arterial blood gases. Forty-eight hours later, two polysomnographic recordings were performed during nPSV 15/4 cmH 2 O, before and after C-fiber blockade. During nPSV, blockade of C-fibers did not prevent inspiratory EaTA (present for 74 ± 41% of respiratory cycles vs. 64 ± 35%, p = 0.9). We conclude that active inspiratory laryngeal narrowing during nPSV does not originate from bronchopulmonary C-fiber endings.

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“…The afferent activity arising from C-fiber endings plays an important role in regulating respiratory functions under both normal and pathophysiologic conditions. Capsaicin, a pungent ingredient of chili peppers, is known to activate airway C-fibers, and this activation has long been associated with the initiation of several central reflexes, including increases in respiratory rate, parasympathetic bronchoconstriction, mucus hypersecretion, vasodilation, as well as urge to cough sensations and sensations of dyspnea [2,3].…”

Section: Introductionmentioning

confidence: 99%

Is TRPV1 a useful target in respiratory diseases?

Takemura

Quarcoo

Niimi

et al. 2008

Pulmonary Pharmacology & Therapeutics

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This review focuses on the transient receptor potential vanilloid 1 (TRPV1). TRPV1 is a non-selective cation channel predominantly expressed in the cell membranes of sensory afferent fibers, which are activated multi-modally. In the mammalian respiratory system, immunohistochemical and electrophysiological studies have revealed heterogeneous localizations of TRPV1 channels in the airways and their presence in pleural afferents. TRPV1 channels in afferents are not only involved with sensory inputs, but also release several neuropeptides upon stimulation. These processes trigger pathophysiological effects (e.g. reflex bronchoconstriction, hypersecretion, cough, etc.) that cause various symptoms of airway diseases.Recent studies have identified several endogenous and exogenous substances that can activate TRPV1 in the lung. Because of its key role in initiating inflammatory processes, TRPV1 receptor antagonists have been proposed as therapeutic candidates. Therefore, a critical update of recent therapeutic results is also given in this review.

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Afferent vagal C fibre innervation of the lungs and airways and its functional significance

Cited by 607 publications

References 205 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

Laryngeal narrowing during nasal ventilation does not originate from bronchopulmonary C-fibers

Is TRPV1 a useful target in respiratory diseases?

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