Effects of emorfazone on the nociceptive response induced by bradykinin in rats and dogs.

Effects of emorfazone on the nociceptive responses induced by the liminal dose of bradykinin (BK alone-induced response), the combined use of the subliminal dose of BK and prostaglandin E (PGE-potentiated response) and the electrical stimulation of the sensory nerve were investigated. BK and PGE were injected into the femoral artery of dogs and the right common carotid artery of rats. In lightly anesthetized dogs, emorfazone (5-20 mg/kg, i.v.), aminopyrine (30 mg/kg, i.v.) and aspirin (50 mg/kg, i.v.) inhibited the vocalization response induced by BK alone but did not by the electrical stimulation of the saphenous nerve. Unlike morphine hydrochloride, these drugs showed a blocking action on the saphenous nerve activity evoked by BK. However, these three drugs differed from each other with respect to the action on the PGE-potentiated response; emorfazone inhibited the PGE-potentiated response to the same extent as in the case of the BK alone-induced response, while aminopyrine was more less active in inhibiting the PGE-potentiated response than BK alone-induced response and aspirin showed no action on the PGE-potentiated response. Such mode of action of emorfazone on BK-induced nociception was confirmed with a similar experiment using conscious rats. These results suggest that the main site of anti-nociceptive action of emorfazone may be in the periphery, and that its action may be not due to inhibition of PGs-synthesis or release.