Laneuville O, Couture R
Eur J Pharmacol. 1987 Jun 4;137(2-3):281-5. doi: 10.1016/0014-2999(87)90237-8.
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.
在清醒受限的大鼠中，鞘内注射81皮摩尔至8.1纳摩尔的缓激肽（BK）可延长对有害热辐射刺激的反应时间。甩尾潜伏期的延长在给药1分钟时达到峰值，并在BK给药后11 - 16分钟恢复到基础水平。在给予肽后5秒即可观察到行为反应，且持续30 - 45秒。当在鞘内预先给予6.1纳摩尔的[Thi5,8, D - Phe7]BK（一种BK的B2受体拮抗剂）后再给予BK时，潜伏期的延长显著减弱。类似物[Leu8]BK-(1 - 8)（10.3纳摩尔），一种BK的B1受体拮抗剂，未能改变BK诱导的镇痛作用。单独的这两种类似物以及BK片段BK-(1 - 8)（一种BK的B1受体强效刺激剂）均未能改变反应时间，只有B2受体拮抗剂可降低BK诱导的行为反应。这些结果表明，BK可能通过激活脊髓感觉通路中一种B2受体类型在疼痛调节中发挥作用。
