Evidence map›Paper›PMID 22687618›Full record

ArticleThe Journal of physiology2012

A role for ATP in bronchoconstriction-induced activation of guinea pig vagal intrapulmonary C-fibres.

Letitia A Weigand, Anthony P Ford, Bradley J Undem

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

28 citing papers in PubMed, 48 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. Mucins and Their Roles in Asthma.Immunological reviews · 2025
    Review
  6. Vagal Reflexes in Airway Hyperreactivity: Novel Pathways and a Note of Caution for Studies in Mice.American journal of respiratory cell and molecular biology · 2023
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Airway Innervation and Plasticity in Asthma.Physiology (Bethesda, Md.) · 2019
    Review
  19. Review
  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 1 institution in 1 country.

Letitia A WeigandJohns Hopkins University School of Medicine, The Johns Hopkins Asthma and Allergy Center, 5501 Hopkins Bayview Circle 1A62, Baltimore, MD21224, USA.
Anthony P Ford
Bradley J Undem
Johns Hopkins University · US

Funding

Airway Sensory NeuroexcitabilityR01HL062296 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI UNDEM, BRADLEY JOEL · 2000 to 2013
$5.0M
Mechanisms of Inflammatory Activation of Vagal C-Fibers in the Respiratory TractR01HL137807 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI UNDEM, BRADLEY JOEL · 2017 to 2020
$1.6M
NHLBI NIH HHS IF31HL099635-01NHLBI NIH HHS R01 HL062296NHLBI NIH HHS R01HL062296NHLBI NIH HHS R01 HL137807
6 · The paper itself

Abstract

Activation of vagal afferent sensory C-fibres in the lungs leads to reflex responses that produce many of the symptoms associated with airway allergy. There are two subtypes of respiratory C-fibres whose cell bodies reside within two distinct ganglia, the nodose and jugular, and whose properties allow for differing responses to stimuli. We here used extracellular recording of action potentials in an ex vivo isolated, perfused lung-nerve preparation to study the electrical activity of nodose C-fibres in response to bronchoconstriction. We found that treatment with both histamine and methacholine caused strong increases in tracheal perfusion pressure that were accompanied by action potential discharge in nodose, but not in jugular C-fibres. Both the increase in tracheal perfusion pressure and action potential discharge in response to histamine were significantly reduced by functionally antagonizing the smooth muscle contraction with isoproterenol, or by blocking myosin light chain kinase with ML-7. We further found that pretreatment with AF-353 or 2',3'-O-(2,4,6-Trinitrophenyl)-adenosine-5'-triphosphate (TNP-ATP), structurally distinct P2X3 and P2X2/3 purinoceptor antagonists, blocked the bronchoconstriction-induced nodose C-fibre discharge. Likewise, treatment with the ATPase apyrase, in the presence of the adenosine A1 and A2 receptor antagonists 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) and SCH 58261, blocked the C-fibre response to histamine, without inhibiting the bronchoconstriction. These results suggest that ATP released within the tissues in response to bronchoconstriction plays a pivotal role in the mechanical activation of nodose C-fibres.

Indexed as

Action PotentialsAdenosine A1 Receptor AntagonistsAdenosine A2 Receptor AntagonistsAdenosine TriphosphateAnimalsApyraseBronchial SpasmGuinea PigsHistamineMaleMethacholine ChlorideNodose GanglionPurinergic P2X Receptor AntagonistsReceptor, Adenosine A1Receptors, Adenosine A2Receptors, Purinergic P2XAdenosine A1 Receptor AntagonistsAdenosine A2 Receptor AntagonistsAdenosine TriphosphateApyraseHistamineMethacholine ChloridePurinergic P2X Receptor AntagonistsReceptor, Adenosine A1Receptors, Adenosine A2Receptors, Purinergic P2X

Identifiers

PMID22687618
PMCPMC3476651
OpenAlexW1577961500

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.