Taiwo Y O, Levine J D
Department of Medicine, University of California, San Francisco 94143.
Brain Res. 1988 Aug 23;458(2):402-6. doi: 10.1016/0006-8993(88)90487-8.
It has been suggested that bradykinin (BK) and norepinephrine (NE) induce hyperalgesia, indirectly, by stimulating the production of prostaglandin products of the cyclo-oxygenase pathway of arachidonic acid metabolism. However, the specific PGs that mediate the hyperalgesic effects of BK and NE are unknown. Two endogenous PGs, prostaglandin E2 (PGE2) and prostacyclin (PGI2) are known to produced hyperalgesia. Since the hyperalgesic effects of PGE2 and PGI2 can be distinguished by the duration of the hyperalgesia they induce, we have compared the duration of BK and NE hyperalgesia with those of PGE2 and PGI2. To further address the type of PG mediating BK and NE hyperalgesia, we have evaluated the ability of SC19220, a PG-receptor antagonist, to distinguish the hyperalgesia induced by PGE2 and PGI2. BK induces hyperalgesia with duration similar to that of PGE2. NE induces hyperalgesia with duration similar to that of PGI2. SC19220, at low doses, antagonizes PGE2 and BK hyperalgesia but not PGI2 and NE hyperalgesia. These data are compatible with the suggestion that the prostaglandin products mediating BK and NE hyperalgesia differ, BK hyperalgesia being mediated by PGE2 and NE hyperalgesia by PGI2.
