Banik Ratan Kumar, Sato Jun, Giron Rocio, Yajima Hiroki, Mizumura Kazue
Department of Neural Regulation, Research Institute of Environmental Medicine, Nagoya University, Furo, Chikusa, Nagoya 464-8601, Japan.
Neurosci Res. 2004 Aug;49(4):421-5. doi: 10.1016/j.neures.2004.05.002.
Many inflammatory chemical mediators excite or sensitize nociceptors, which had led some researchers to believe that they may interact with each other to maintain a persistent painful state. We examined how the excitatory mediators norepinephrine (NE) and bradykinin (BK) interact, using single fiber recordings from cutaneous nociceptors. We observed that NE augmented the BK-induced response in both control and adjuvant-inflamed rats in a way different from NE-induced excitation in inflamed animals only. BK also tended to augment the NE-induced response (examined only in inflamed rats). Our results provide the first evidence that BK and NE synergistically interact on nociceptors.
许多炎症化学介质会刺激伤害感受器或使其敏感化,这使得一些研究人员认为它们可能相互作用以维持持续的疼痛状态。我们使用皮肤伤害感受器的单纤维记录,研究了兴奋性介质去甲肾上腺素(NE)和缓激肽(BK)如何相互作用。我们观察到,在对照大鼠和佐剂诱导炎症的大鼠中,NE均以一种不同于仅在炎症动物中NE诱导兴奋的方式增强了BK诱导的反应。BK也倾向于增强NE诱导的反应(仅在炎症大鼠中进行了检测)。我们的结果首次证明了BK和NE在伤害感受器上存在协同相互作用。