Bradykinin analogue blocks bradykinin-induced inhibition of a spinal nociceptive reflex in the rat.
In the awake restrained rat the intrathecal (i.th.) administration of 81 pmol to 8.1 nmol of bradykinin (BK) increased reaction time to a noxious radiant heat stimulus. The enhancement of tail-flick latency peaked at 1 min and returned to the basal level 11-16 min after BK administration. Behavioural responses were observed as early as 5 s following peptide administration and lasted for 30-45 s. When BK was given after prior i.th. administration of 6.1 nmol of [Thi5,8, D-Phe7]BK, an antagonist of BK at the B2-receptor, the increase in latency was significantly attenuated. The analogue [Leu8]BK-(1-8) (10.3 nmol), an antagonist of BK at the B1-receptor, failed to modify the BK-induced antinociception. The two analogues alone and the fragment BK-(1-8), a potent stimulant of B1-receptors for BK, failed to alter reaction time and only the B2-receptor antagonist reduced BK-induced behavioural responses. These results suggest that BK may play a role through the activation of a B2-receptor type in a spinal sensory pathway subserving pain.
D000818:Animals; D001920:Bradykinin / Q000031:analogs & derivatives* / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D008297:Male; D009619:Nociceptors / Q000187:drug effects*; D051381:Rats; D011919:Rats, Inbred Strains; D011930:Reaction Time / Q000187:drug effects; D012018:Reflex / Q000187:drug effects*; D013116:Spinal Cord / Q000187:drug effects*
C051090:bradykinin, Leu(8)-des-Arg(9)-; C053426:bradykinin, (Thi-Ala)(5,8)-Phe(7)-; D001920:Bradykinin