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 Neuroscijournal_title
Trends in neurosciencesauthors
Dray A,Perkins Mdoi
10.1016/0166-2236(93)90133-7subject
Has Abstractpub_date
1993-03-01 00:00:00pages
99-104issue
3eissn
0166-2236issn
1878-108Xpii
0166-2236(93)90133-7journal_volume
16pub_type
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更新日期:2000-07-01 00:00:00
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更新日期:2001-02-01 00:00:00
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pub_type: 杂志文章,评审
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