Bradykinin and inflammatory pain

  title={Bradykinin and inflammatory pain},
  author={Andy Dray and Martin N. Perkins},
  journal={Trends in Neurosciences},

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Bradykinin, Cytokines and Inflammatory Hyperalgesia

Bradykinin and related peptides are produced at sites of tissue injury and inflammation and have an important role in mediating the responses of the tissues to damage and associated pain, notably when the hyperalgesia is secondary to an earlier inflammatory insult.

Kinins and their receptors in hyperalgesia.

  • A. Dray
  • Biology, Medicine
    Canadian journal of physiology and pharmacology
  • 1997
The evidence for modulation of nociception and central pain generation is compelling, as central bradykinin administration causes hyperalgesia, whereas B2 antagonists are antinociceptive.

Kinin receptors in pain and inflammation.

Interactions between kinins and the inflammatory pain process

A large number of variants on these two peptides have been identified, such as T kinin which is specific to the rat, and others in man but little is known about their role in the modulation of nociception.

B2 receptor-mediated enhanced bradykinin sensitivity of rat cutaneous C-fiber nociceptors during persistent inflammation.

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.

Bradykinin Antagonists Have No Analgesic Effect on Incisional Pain

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.

Pathogenesis and Mechanisms of Inflammation and Pain

The severe pain that accompanies inflammatory disease such as rheumatoid arthritis is caused by the action of pain-producing substances such as kinins on nociceptor neurons sensitised by locally produced prostaglandins, and perhaps sympathomimetics released from sympathetic nerves.

Excitation and sensitization of nociceptors by bradykinin: what do we know?

Prostaglandins sensitize bradykinin-induced excitation in normal tissues by restoring desensitized responses due to the inhibition of protein kinase A.



Multiple bradykinin receptors: results of studies using a novel class of receptor antagonists.

Results of studies of the effects of the antagonists on bradykinin receptor binding, receptor-coupled transduction systems, isolated smooth muscle, and in vivo animal models of pain and hyperalgesia suggest that pharmacologically distinct types of bradyKinin receptors may exist in different tissues.

Biochemical and molecular pharmacology of kinin receptors.

Recent advances in the understanding of biochemical and molecular aspects of kinin receptor pharmacology are highlighted.

Peripheral Mechanisms of Somatic Pain

It is hoped that future studies in experimental animals, careful psychophysical testing and microneurographic recordings in chronic pain patients, will lead to a better understanding of the pathophysiology of pain.

Peripheral analgesic actions of opioids.

  • C. Stein
  • Biology
    Journal of pain and symptom management
  • 1991

Noradrenaline hyperalgesia is mediated through interaction with sympathetic postgahglionic neurone terminals rather than activation of primary afferent nociceptors

It is demonstrated that the site of action of noradrenaline is not on the primary afferents but rather is presynaptic on the sympathetic post-ganglionic terminals.

Interleukin-1β as a potent hyperalgesic agent antagonized by a tripeptide analogue

An analgesic tripeptide analogue of IL-1β is developed which antagonizes hyperalgesia evoked by IL- 1β and by the inflammatory agent carrageenan.