Bradykinin and inflammatory pain.

Abstract:

: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 and anti-inflammatory agents in acute inflammatory pain. More recently it has been suggested that when inflammation is prolonged, BK B1 receptors, which are not expressed in healthy tissues to a significant degree, also play an important role in the maintenance of hyperalgesia. This may be one of a number of adaptive mechanisms that occur peripherally and centrally following the prolonged activation of nociceptors during inflammation or injury.

journal_name

Trends Neurosci

journal_title

Trends in neurosciences

authors

Dray A,Perkins M

doi

10.1016/0166-2236(93)90133-7

subject

Has Abstract

pub_date

1993-03-01 00:00:00

pages

99-104

issue

3

eissn

0166-2236

issn

1878-108X

pii

0166-2236(93)90133-7

journal_volume

16

pub_type

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