Evidence map›Paper›PMID 15860525›Full record

ArticleThe Journal of physiology2005

Role of chloride channels in bradykinin-induced guinea pig airway vagal C-fibre activation.

Min-Goo Lee, Donald W Macglashan, Bradley J Undem

Open access · greenAbstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.7field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
  2. Review
  3. Role of TRP channels in GAmerican journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  4. Review
  5. Targeting C-fibers for peripheral acting anti-tussive drugs.Pulmonary pharmacology & therapeutics · 2019
    Review
  6. Review
  7. Article
  8. Review
  9. Pharmacology of Bradykinin-Evoked Coughing in Guinea Pigs.The Journal of pharmacology and experimental therapeutics · 2016
    Article
  10. Article
  11. Increased acid responsiveness in vagal sensory neurons in a guinea pig model of eosinophilic esophagitis.American journal of physiology. Gastrointestinal and liver physiology · 2014
    Article
  12. Article
  13. Article
  14. 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 · 2013
    Article
  15. Article
  16. Review
  17. Article
  18. Ionic mechanisms underlying inflammatory mediator-induced sensitization of dural afferents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 1 country.

Min-Goo LeeJohns Hopkins Asthma and Allergy Center, 5501 Hopkins Bayview Circle, Baltimore, MD 21224, USA.
Donald W Macglashan
Bradley J Undem
Johns Hopkins Bayview Medical Center · USJohns Hopkins Medicine · USJohns Hopkins University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Afferent PathwaysAnimalsBradykininCalciumCalcium SignalingChloride ChannelsDose-Response Relationship, DrugGuinea PigsIn Vitro TechniquesIon Channel GatingMaleMembrane PotentialsNeurons, AfferentRespiratory SystemVagus NerveBradykininCalciumChloride Channels

Identifiers

PMID15860525
PMCPMC1464732
OpenAlexW1535198700

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.