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A bradykinin (BK) 1 receptor antagonist blocks capsaicin‐induced ear inflammation in mice
Author(s) -
Mantione Charles R.,
Rodriguez Richard
Publication year - 1990
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1990.tb12960.x
Subject(s) - bradykinin , antagonist , capsaicin , chemistry , receptor antagonist , endocrinology , nk1 receptor antagonist , pharmacology , medicine , receptor , inflammation , neuropeptide , substance p
1 The effect of various peptide antagonists on capsaicin‐induced (250 μg per ear) ear inflammation has been examined. 2 Co‐administration of the substance P (SP) antagonist [ d ‐Pro 2 , d ‐Trp 7,9 ]SP at 100 and 300 μg per ear with capsaicin markedly attenuated oedema, whereas a vasopressin antagonist was ineffective. 3 Using the same scheme, the mixed BK 2 and BK 1 bradykinin (BK) antagonist NPC 567 ( d ‐Arg[Hyp 3 , d ‐Phe 7 ]BK) did not inhibit oedema at 100 μg per ear, but did inhibit at a higher dose (300 μg). The BK 1 antagonist [Leu 8 ,desArg 9 ]BK produced significant inhibition at both doses. 4 When BK was used to induce ear inflammation (30 μg per ear), the SP antagonist inhibited ear oedema. Both BK receptor subtype antagonists inhibited inflammation with the BK 1 being more potent than the BK 2 antagonist. 5 These results suggest that BK 1 along with BK 2 receptors are located on capsaicin‐sensitive fibres, where they may modulate the degree of neurogenic inflammation.