Evidence map›Paper›PMID 20335661›Full record

ArticleThe Journal of clinical investigation2010

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.

Boyi Liu, John E Linley, Xiaona Du, Xuan Zhang, Lezanne Ooi, Hailin Zhang, Nikita Gamper

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 176 papers.

0numbers the graph read from it
0cells of the map it votes in
176citing papers in PubMed
13.3field-weighted citation impact, top 1% 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

176 citing papers in PubMed, 288 citations in OpenAlex.

  1. Progress in pain mechanisms and management.Signal transduction and targeted therapy · 2026
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  3. Cancer pain.Nature reviews. Disease primers · 2026
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  13. Calcium-sensing receptor regulates Kv7 channels via GBritish journal of pharmacology · 2024
    Article
  14. Article
  15. Article
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  17. Article
  18. Article
  19. Article
  20. KAmerican journal of physiology. Gastrointestinal and liver physiology · 2023
    Article

116 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Boyi LiuDepartment of Pharmacology, Hebei Medical University, Shijiazhuang, China.
John E Linley
Xiaona Du
Xuan Zhang
Lezanne Ooi
Hailin Zhang
Nikita Gamper
Hebei Medical University · CN

Funding

Medical Research Council 82507Medical Research Council G0700966Wellcome TrustWellcome Trust 070740Wellcome Trust 080593/Z06/ZWellcome Trust 080833/Z/06/Z
6 · The paper itself

Abstract

Bradykinin (BK) is an inflammatory mediator and one of the most potent endogenous pain-inducing substances. When released at sites of tissue damage or inflammation, or applied exogenously, BK produces acute spontaneous pain and causes hyperalgesia (increased sensitivity to potentially painful stimuli). The mechanisms underlying spontaneous pain induced by BK are poorly understood. Here we report that in small nociceptive neurons from rat dorsal root ganglia, BK, acting through its B2 receptors, PLC, and release of calcium from intracellular stores, robustly inhibits M-type K+ channels and opens Ca2+-activated Cl- channels (CaCCs) encoded by Tmem16a (also known as Ano1). Summation of these two effects accounted for the depolarization and increase in AP firing induced by BK in DRG neurons. Local injection of inhibitors of CaCC and specific M-channel openers both strongly attenuated the nociceptive effect of local injections of BK in rats. These results provide a framework for understanding spontaneous inflammatory pain and may suggest new drug targets for treatment of such pain.

Indexed as

AnimalsBradykininCalciumChloride ChannelsGanglia, SpinalNociceptorsPainPotassium Channel BlockersRatsRats, Sprague-DawleyRats, WistarReceptor, Bradykinin B2Sensory Receptor CellsSignal TransductionBradykininCalciumChloride ChannelsPotassium Channel BlockersReceptor, Bradykinin B2

Identifiers

PMID20335661
PMCPMC2846053
OpenAlexW2096242779

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.