Bradykinin and inflammatory pain

@article{Dray1993BradykininAI,
  title={Bradykinin and inflammatory pain},
  author={Andy Dray and Martin N. Perkins},
  journal={Trends in Neurosciences},
  year={1993},
  volume={16},
  pages={99-104}
}
There is compelling evidence linking bradykinin (BK) with the pathophysiological processes that accompany tissue damage and inflammation, especially the production of pain and hyperalgesia. Several mechanisms have been proposed to account for hyperalgesia including the direct activation of nociceptors as well as sensitization of nociceptors through the production of prostanoids or the release of other mediators. In keeping with this, antagonists of the BK B2 receptor are efficacious analgesic… Expand
Bradykinin, Cytokines and Inflammatory Hyperalgesia
TLDR
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Kinins and their receptors in hyperalgesia.
  • A. Dray
  • Medicine
  • Canadian journal of physiology and pharmacology
  • 1997
TLDR
The evidence for modulation of nociception and central pain generation is compelling, as central bradykinin administration causes hyperalgesia, whereas B2 antagonists are antinociceptive. Expand
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TLDR
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TLDR
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TLDR
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Kinins and Pain
Publisher Summary This chapter provides an overview of the kinins and pain. Pain signals are generated in fine afferent C- and Aδ nerve fibers, which respond to a range of intense physiologicalExpand
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There is now a substantial body of evidence to suggest that kinins play a major role in the initiation and maintenance of the inflammatory pain process. Kinins are small peptides, sometimes calledExpand
B2 receptor-mediated enhanced bradykinin sensitivity of rat cutaneous C-fiber nociceptors during persistent inflammation.
TLDR
In chronically inflamed tissue, sensitivity of C-fiber nociceptors to BK, which is B2 receptor mediated, is strongly increased and B1 receptor may not be important to a persistent inflammatory state, at least at the primary afferent level. Expand
Bradykinin Antagonists Have No Analgesic Effect on Incisional Pain
TLDR
None of the doses of either dALBK or HOE-140 affected the responses to punctate or blunt mechanical stimulation or heat, either as a pretreatment or as a posttreatment, which support the unique mechanisms for incision-induced pain relative to inflammation-related pain. Expand
Some new insights into the molecular mechanisms of pain perception.
TLDR
The relationship between the stimulation of B2 bradykinin receptors and a previously described mechanism for pain sensitization and its potential significance for therapeutic pain control are discussed. Expand
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TLDR
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TLDR
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