Evidence map›Paper›PMID 10859349›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2000

Hypoalgesia and altered inflammatory responses in mice lacking kinin B1 receptors.

J B Pesquero, R C Araujo, P A Heppenstall, C L Stucky, J A Silva, T Walther, S M Oliveira, J L Pesquero, A C Paiva, J B Calixto and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 1 pooled it
14.4field-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

90 citing papers in PubMed, 1 synthesis or guideline pooled it, 376 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Theranostic Potential of a NewPharmaceutics · 2025
    Article
  6. Article
  7. Kinin B1 receptor deficiency promotes enhanced adipose tissue thermogenic response to β3-adrenergic stimulation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  8. Article
  9. Kinins: Locally formed peptides during inflammation with potential use in tissue regeneration.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  10. Article
  11. Kinin receptors regulate skeletal muscle regeneration: differential effects for B1 and B2 receptors.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  12. Article
  13. A compendium of validated pain genes.WIREs mechanisms of disease · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Kinins and Kinin Receptors in Cardiovascular and Renal Diseases.Pharmaceuticals (Basel, Switzerland) · 2021
    Review
  19. BBritish journal of pharmacology · 2020
    Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 1 institution in 1 country.

J B PesqueroMolecular Biology of Peptide Hormones Group, and Growth Factors and Regeneration Group in the Department of Neuroscience, Max Delbrück Center for Molecular Medicine, D-13092 Berlin-Buch, Germany.
R C Araujo
P A Heppenstall
C L Stucky
J A Silva
T Walther
S M Oliveira
J L Pesquero
A C Paiva
J B Calixto
G R Lewin
M Bader
Universidade Federal de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kinins are important mediators in cardiovascular homeostasis, inflammation, and nociception. Two kinin receptors have been described, B1 and B2. The B2 receptor is constitutively expressed, and its targeted disruption leads to salt-sensitive hypertension and altered nociception. The B1 receptor is a heptahelical receptor distinct from the B2 receptor in that it is highly inducible by inflammatory mediators such as bacterial lipopolysaccharide and interleukins. To clarify its physiological function, we have generated mice with a targeted deletion of the gene for the B1 receptor. B1 receptor-deficient animals are healthy, fertile, and normotensive. In these mice, bacterial lipopolysaccharide-induced hypotension is blunted, and there is a reduced accumulation of polymorphonuclear leukocytes in inflamed tissue. Moreover, under normal noninflamed conditions, they are analgesic in behavioral tests of chemical and thermal nociception. Using whole-cell patch-clamp recordings, we show that the B1 receptor was not necessary for regulating the noxious heat sensitivity of isolated nociceptors. However, by using an in vitro preparation, we could show that functional B1 receptors are present in the spinal cord, and their activation can facilitate a nociceptive reflex. Furthermore, in B1 receptor-deficient mice, we observed a reduction in the activity-dependent facilitation (wind-up) of a nociceptive spinal reflex. Thus, the kinin B1 receptor plays an essential physiological role in the initiation of inflammatory responses and the modulation of spinal cord plasticity that underlies the central component of pain. The B1 receptor therefore represents a useful pharmacological target especially for the treatment of inflammatory disorders and pain.

Indexed as

AnimalsBlood PressureElectric StimulationHot TemperatureInflammationMiceMice, KnockoutNeurons, AfferentPainPain ThresholdReceptor, Bradykinin B1Receptors, BradykininReflexSpinal CordStimulation, ChemicalReceptor, Bradykinin B1Receptors, Bradykinin

Identifiers

PMID10859349
PMCPMC16683
OpenAlexW2148390754

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.