The role of bradykinin receptors in activating and sensitizing nociceptors in the periphery is well known. Recently, our studies have suggested that the pronociceptive actions of dynorphin in the central nervous system are the result of a novel interaction with bradykinin receptors. Blockade of bradykinin receptors reversed nerve injury-induced tactile and thermal hyperalgesia only at times at which spinal levels of dynorphin were elevated. The present study explored the role of bradykinin receptors in visceral pain using a model of chronic pancreatitis induced by intravenous injection of dibutyltin dichloride (DBTC) in rats. DBTC produced sustained abdominal hypersensitivity over the course of several days. Following DBTC, RT-PCR analysis revealed up-regulation of bradykinin B2, but not B1, receptors in the pancreas, increased levels of both B1 and B2 receptors in the thoracic DRG, but no changes in bradykinin receptor expression in the spinal cord. Intraperitoneal administration of HOE 140, a B2 antagonist, produced dose-dependent reversal of abdominal hypersensitivity in rats with pancreatitis on day 7 post DBTC; Des-Arg9-Leu8-bradykinin, a B1 receptor antagonist had no effect. Intrathecal injection at the thoracic spinal level of HOE 140 also elicited a dose-related inhibition of pancreatitis pain while the B1 antagonist had no effect. DBTC produced an upregulation of spinal dynorphin and spinal administration of antiserum to dynorphin also produced a reversal of pancreatitis pain. These results suggest a functional role for bradykinin B2 receptor expressed in the periphery. Additionally, the data suggest a role for spinal dynorphin in maintaining pancreatitis pain through actions at bradykinin B2 receptors. Selective B2 antagonists which penetrate the CNS may therefore have therapeutic potential against pancreatitis pain through both peripheral and central sites and mechanisms of action.