Central nervous system activity associated with the pain evoked by bradykinin and its alteration by morphine and aspirin.

Synthetic bradykinin, a nonapeptide formed from alpha-2 globulin in plasma, injected intra-arterially or intraperitoneally in cats in doses of 10-50 mug, evoked activity in the central nervous system in pathways associated with the signaling of pain. Similar injections of bradykinin in intact normal cats and dogs evoked manifestations of pain, and in conscious humans elicited verbal reports of pain perceived in the area of injection. Single unit activity was recorded in the medial reticular formation of the brainstem, in the medial thalamus and, more laterally, among the posterior group nuclei and the suprageniculate nucleus. Bradykinin did not evoke any cortical or subcortical slow potentials such as those evoked by electrical stimulation of the foot pads. When bradykinin was given together with the electrical stimulus, the responses evoked by the latter were blocked. Morphines uppressed bradykinin-evoked activity. Aspirin caused marked fluctuations in activity, unrelated to the bradykinin injection; the bradykinin block of evoked potentials could no longer be observed after aspirin dosage. The results are discussed in terms of the peripheral and central sites of analgesic action and the likelihood of the existence of chemosensitive pain receptors.