The ability of Bothrops asper snake venom to cause hyperalgesia was investigated in rats, using the paw pressure test. Intraplantar injection of the venom (5-15 microg/paw) caused a dose and time-related hyperalgesia, which peaked 2h after venom injection. Bothrops asper venom-induced hyperalgesia was blocked by the bradykinin B(2) receptor antagonist HOE 140 and attenuated by dexamethasone, an inhibitor of phospholipase A(2). Inhibition of the lipoxygenase pathway by NDGA abrogated the algogenic phenomenon. The hyperalgesic response was not modified by pretreatment with indomethacin, an inhibitor of the cyclo-oxygenase pathway, by meloxicam, an inhibitor of the type 2 cyclo-oxygenase pathway, by the PAF receptor antagonist BN52021 or by anti-TNF-alpha or anti-interleukin 1 antibodies. Intraplantar injection of the venom also caused an oedematogenic response which was not modified by any of these pharmacological treatments. These results suggest that hyperalgesia induced by Bothrops asper venom is, at least partially, mediated by bradykinin, phospholipase A(2) activity and leukotrienes. Distinct mechanisms are involved in the development of hyperalgesia and oedema induced by the venom.