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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.
K Messlinger, and
K Schepelmann, and
M Pawlak, and
R F Schmidt
May 1997,
European journal of pharmacology,
K Messlinger, and
K Schepelmann, and
M Pawlak, and
R F Schmidt
March 2012,
Journal of medicinal chemistry,
K Messlinger, and
K Schepelmann, and
M Pawlak, and
R F Schmidt
December 1994,
Brain research,
K Messlinger, and
K Schepelmann, and
M Pawlak, and
R F Schmidt
December 1994,
Pain,
K Messlinger, and
K Schepelmann, and
M Pawlak, and
R F Schmidt
April 1990,
Trends in pharmacological sciences,
K Messlinger, and
K Schepelmann, and
M Pawlak, and
R F Schmidt
July 1996,
Pain,
K Messlinger, and
K Schepelmann, and
M Pawlak, and
R F Schmidt
January 2003,
European journal of pharmacology,
K Messlinger, and
K Schepelmann, and
M Pawlak, and
R F Schmidt
July 1995,
Canadian journal of physiology and pharmacology,
K Messlinger, and
K Schepelmann, and
M Pawlak, and
R F Schmidt
January 1991,
Hypertension (Dallas, Tex. : 1979),
K Messlinger, and
K Schepelmann, and
M Pawlak, and
R F Schmidt
April 1984,
Annals of the rheumatic diseases,
