Bradykinin release of TNF-alpha plays a key role in the development of inflammatory hyperalgesia.
Using specific antisera for IL-1 beta 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-1 beta and IL-8 is preceded by the liberation of TNF-alpha. 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-alpha 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.
Ferreira
S H
SH
Faculty of Medicine of Ribeirão Preto, Brazil.
Lorenzetti
B B
BB
Cunha
F Q
FQ
Poole
S
S
D000818:Animals; D001920:Bradykinin / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D006614:Hindlimb; D006930:Hyperalgesia / Q000139:chemically induced / Q000209:etiology*; D007213:Indomethacin / Q000494:pharmacology; D007249:Inflammation / Q000139:chemically induced / Q000209:etiology*; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D014409:Tumor Necrosis Factor-alpha; D011433:Propranolol; D001920:Bradykinin; D007213:Indomethacin