ArticleThe Journal of physiology2005
Role of chloride channels in bradykinin-induced guinea pig airway vagal C-fibre activation.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 61 citations in OpenAlex.
- Neural control of the lower airways: Role in cough and airway inflammatory disease.Handbook of clinical neurology · 2022Review
- Molecular identity, anatomy, gene expression and function of neural crest vs. placode-derived nociceptors in the lower airways.Neuroscience letters · 2021Review
- Role of TRP channels in GAmerican journal of physiology. Lung cellular and molecular physiology · 2020Article
- Molecular/Ionic Basis of Vagal Bronchopulmonary C-Fiber Activation by Inflammatory Mediators.Physiology (Bethesda, Md.) · 2020Review
- Targeting C-fibers for peripheral acting anti-tussive drugs.Pulmonary pharmacology & therapeutics · 2019Review
- Depolarizing Effectors of Bradykinin Signaling in Nociceptor Excitation in Pain Perception.Biomolecules & therapeutics · 2018Review
- Mechanisms of pruritogen-induced activation of itch nerves in isolated mouse skin.The Journal of physiology · 2017Article
- Vagal Afferent Innervation of the Airways in Health and Disease.Physiological reviews · 2016Review
- Pharmacology of Bradykinin-Evoked Coughing in Guinea Pigs.The Journal of pharmacology and experimental therapeutics · 2016Article
- Article
- Increased acid responsiveness in vagal sensory neurons in a guinea pig model of eosinophilic esophagitis.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- Anoctamin 1 mediates thermal pain as a heat sensor.Current neuropharmacology · 2013Article
- Store-operated calcium entry in vagal sensory nerves is independent of Orai channels.Brain research · 2013Article
- Bradykinin-induced chemotaxis of human gliomas requires the activation of KCa3.1 and ClC-3.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Direct activation of guinea pig vagal afferent neurons by FMRFamide.Neuroreport · 2011Article
- Targeting peripheral afferent nerve terminals for cough and dyspnea.Current opinion in pharmacology · 2011Review
- Transgene expression and effective gene silencing in vagal afferent neurons in vivo using recombinant adeno-associated virus vectors.The Journal of physiology · 2010Article
- Ionic mechanisms underlying inflammatory mediator-induced sensitization of dural afferents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- The acute nociceptive signals induced by bradykinin in rat sensory neurons are mediated by inhibition of M-type K+ channels and activation of Ca2+-activated Cl- channels.The Journal of clinical investigation · 2010Article
- Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We tested the hypothesis that an ionic current carried by chloride ions contributes to bradykinin (BK)-induced membrane depolarization and activation of vagal afferent C-fibres. In an ex vivo innervated trachea/bronchus preparation, BK (1 microM) consistently produced action potential discharge in vagal afferent C-fibres with receptive fields in the trachea or main stem bronchus. The Ca2+-activated Cl- channel (CLCA) inhibitor, niflumic acid (NFA, 100 microM), significantly reduced BK-induced action potential discharge to 21 +/- 7% of the control BK response. NFA did not inhibit capsaicin-induced or citric-acid-induced action potential discharge in tracheal C-fibres. The inhibitory effect of NFA was mimicked by another CLCA inhibitor, 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB, 100 microM). NFA also inhibited the BK-induced inward current in gramicidin-perforated whole-cell patch-clamp recordings of capsaicin-sensitive jugular ganglion neurones retrogradely labelled from the airways. NFA did not inhibit the BK-induced increase in intracellular free Ca2+. The TRPV1 inhibitor, iodo-resiniferatoxin (1 microM), also partially inhibited BK-induced action potential discharge, and the combination of iodo-resiniferatoxin and NFA virtually abolished the BK-induced action potential discharge. We concluded that in vagal afferent C-fibres, BK evokes membrane depolarization and action potential discharge through the additive effects of TRPV1 and Cl- channel activation.
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