Abstract
Using specific antisera for IL-1β and IL-8, as well as cyclooxygenase inhibitors and propranolol, we have demonstrated that these cytokines are responsible for the prostaglandin and sympathetic components of carrageenin-induced hyperalgesia in the rat paw test. The release of IL-1β and IL-8 is preceded by the liberation of TNF-α. We have also tested in a nociceptive model the effects of bradykinin and a specific bradykinin antagonist, HOE 140, on the hyperalgesia induced by carrageenin and lipopolysaccharide (LPS). Bradykinin-induced hyperalgesia was abolished by HOE 140 and by treatment of the paws with anti-TNF-α antisera. HOE 140 significantly inhibited the hyperalgesia induced by carrageenin and LPS. It is suggested that in these two models bradykinin is associated with the release of hyperalgesic cytokines.
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Ferreira, S.H., Lorenzetti, B.B., Cunha, F.Q. et al. Bradykinin release of TNF-α plays a key role in the development of inflammatory hyperalgesia. Agents and Actions 38 (Suppl 2), C7–C9 (1993). https://doi.org/10.1007/BF01991120
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DOI: https://doi.org/10.1007/BF01991120