Abstract
1. The effect of various peptide antagonists on capsaicin-induced (250 micrograms per ear) ear inflammation has been examined. 2. Co-administration of the substance P (SP) antagonist [D-Pro2,D-Trp7,9]SP at 100 and 300 micrograms per ear with capsaicin markedly attenuated oedema, whereas a vasopressin antagonist was ineffective. 3. Using the same scheme, the mixed BK2 and BK1 bradykinin (BK) antagonist NPC 567 (D-Arg[Hyp3,D-Phe7]BK) did not inhibit oedema at 100 micrograms per ear, but did inhibit at a higher dose (300 micrograms). The BK1 antagonist [Leu8,desArg9]BK produced significant inhibition at both doses. 4. When BK was used to induce ear inflammation (30 micrograms per ear), the SP antagonist inhibited ear oedema. Both BK receptor subtype antagonists inhibited inflammation with the BK1 being more potent than the BK2 antagonist. 5. These results suggest that BK1 along with BK2 receptors are located on capsaicin-sensitive fibres, where they may modulate the degree of neurogenic inflammation.