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Bradykinin release of TNF-α plays a key role in the development of inflammatory hyperalgesia

  • Neurogenic Pain and Inflammation
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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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Authors and Affiliations

  1. Faculty of Medicine of Ribeirão Preto, 14049, Ribeirão Preto, Brazil

    S. H. Ferreira, B. B. Lorenzetti, F. Q. Cunha & S. Poole

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  1. S. H. Ferreira
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  2. B. B. Lorenzetti
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  3. F. Q. Cunha
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  4. S. Poole
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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

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