The peripheral injection of phorbol myristate acetate (PMA) into the mouse paw induces nociception mediated through activation of protein kinase C (PKC). In the present study, we examine the contribution of kinin B1 receptor to PMA-induced nociception. Nociception was assessed after intraplantar injection of PMA or the B1 receptor agonist des-Arg9-bradykinin in mice. Mechanisms of nociception were studied using the combination of knockout mice, selective drugs, and measurement of B1 receptor mRNA and protein levels. Peripheral injection of PMA (50 pmol/paw) induced a nociceptive behaviour that was abolished by selective B1 receptor antagonist des-Arg9-Leu8-bradykinin or by the B1 receptor gene deletion. Moreover, PMA treatment did not alter B1 receptor mRNA levels, but greatly increased B1 receptor protein levels in the mouse paw. The injection of des-Arg9-bradykinin did not cause nociception in naive mice, but produced marked nociception in animals previously treated with a low dose of PMA (0.5 nmol/paw). The co-treatment of PMA with selective PKC or protein synthesis inhibitors, but not with p38 mitogen activated protein kinase (MAPK) or transcription inhibitors significantly reduced des-Arg9-bradykinin-induced nociception. On the other hand, the co-administration of selective PKC or p38 MAPK inhibitors, but not of protein synthesis or transcription inhibitors, reduced des-Arg9-bradykinin-induced nociception when evaluated in PMA pre-injected animals. These results suggest that the B1 receptor exerts a critical role in the nociception caused by PKC activation in peripheral tissues. Since the PKC pathway is downstream of several pro-inflammatory mediators, B1 receptor stimulation appears to contribute to the acute inflammatory pain process.