1 This study was designed to investigate the role of bradykinin (BK), as well as the subtype of BK receptors involved, in formalin-induced hindpaw pain in the mouse by use of selective B, and B2 receptor antagonists. In addition, we have analysed whether or not BK may be involved in formalininduced hindpaw oedema in the mouse. 2 The pretreatment of animals with captopril (2 and 5 mg kg-', s.c.) significantly increase the first and the second phases of formalin-induced pain. significant inhibitions of both phases of formalin-induced pain. When Hoe 140 was injected subcutaneously 30 min before formalin injection (9.9 and 99 nmol kg-'), it significantly attenuated both phases of formalin-induced pain. The putative non-peptide BK antagonist, MV 8612 (1.6 to 9.6 nmol/ paw), but not MV 8608 (5.5 to 33 nmol/paw), caused a graded inhibition of both phases of formalininduced pain, being, however, more active against the first phase.5 The pretreatment of animals with morphine (2.6 to 13 #zmol kg-', s.c.) caused dose-dependent and equipotent inhibitions of both phases of formalin-induced pain. In contrast, indomethacin (2.7 to 27 limol kg -) antagonized only the second phase of formalin-induced pain.6 The B2 receptor antagonists, Hoe 140, NPC 17731, NPC 17761, NPC 349 and NPC 567, all caused a significant inhibition of formalin-induced hindpaw oedema. A similar inhibition was also observed with indomethacin but not with captopril or morphine. 7 Our results provide strong evidence for the important role of endogenous BK, acting through both B, and B2 receptors, in the genesis of both phases of formalin-induced persistent pain in the mouse. In addition, the current results also demonstrate that the inflammatory oedema associated with the later phase of formalin-induced pain seems to be mediated by endogenous BK, via activation of B2 receptors.