Bradykinin B1 and B2 receptor antagonists do not change the ongoing activity of slowly conducting articular afferents in the inflamed knee joint of the cat.
Arthritic hyperalgesia and pain result from an increased activity of nociceptive afferents that may be induced and maintained by inflammatory mediators like bradykinin (BK). The B1 receptor antagonist des-Arg9-Leu8-BK and the B2 receptor antagonists Thi5,8-D-Phe7-BK and Hoe 140 were used to study the involvement of BK receptors in the generation of ongoing afferent activity in the cat's knee joint that was inflamed by kaolin and carrageenin. After i.a. bolus administration of BK receptor antagonists (26-260 micrograms) close to the joint, the ongoing activity did not significantly vary in any group III or group IV unit. We conclude that activation of BK receptors by endogenous BK is probably not the mechanism that is responsible for the increased ongoing activity of articular afferents in the inflamed joint.
Messlinger
K
K
Physiologisches Institut, Universität Würzburg, Germany.
Schepelmann
K
K
Pawlak
M
M
Schmidt
R F
RF
D000818:Animals; D001169:Arthritis, Experimental / Q000503:physiopathology*; D001920:Bradykinin / Q000031:analogs & derivatives / Q000494:pharmacology; D065168:Bradykinin Receptor Antagonists; D002415:Cats; D006614:Hindlimb / Q000502:physiology; D009431:Neural Conduction / Q000187:drug effects / Q000502:physiology; D009475:Neurons, Afferent / Q000187:drug effects*; D009619:Nociceptors / Q000502:physiology; D011189:Potassium Chloride / Q000494:pharmacology
D065168:Bradykinin Receptor Antagonists; C058532:HOE k86-4321; D011189:Potassium Chloride; C065679:icatibant; D001920:Bradykinin