Chahl L A, Chahl J S
Eur J Pharmacol. 1986 May 27;124(3):343-7. doi: 10.1016/0014-2999(86)90237-2.
The plasma extravasation response to dynorphin-(1-13) was investigated using the Evans blue dye leakage technique. Dynorphin induced plasma extravasation in rat and guinea-pig abdominal skin with a similar potency to substance P. In rat skin dynorphin, unlike substance P, produced its action entirely by release of histamine and 5-hydroxytryptamine since the response was abolished by pretreatment of rats with mepyramine and methysergide. Pretreatment of rats with capsaicin or the tachykinin antagonist, spantide, reduced but did not abolish the response to dynorphin, indicating that its action was not mediated primarily by a neurogenic mechanism. Since the response was not significantly reduced by naloxone it was concluded that the plasma extravasation response to dynorphin was mediated by receptors other than mu opiate receptors. Thus dynorphin, if released from sensory nerves, might play a role in neurogenic inflammation.
采用伊文思蓝染料渗漏技术研究了强啡肽-（1-13）引起的血浆外渗反应。强啡肽在大鼠和豚鼠腹部皮肤中诱导血浆外渗，其效力与P物质相似。在大鼠皮肤中，与P物质不同，强啡肽完全通过组胺和5-羟色胺的释放发挥作用，因为用甲氧苄二胺和甲基麦角新碱预处理大鼠可消除该反应。用辣椒素或速激肽拮抗剂spantide预处理大鼠可降低但不能消除对强啡肽的反应，表明其作用并非主要由神经源性机制介导。由于纳洛酮并未显著降低该反应，因此得出结论，强啡肽引起的血浆外渗反应是由μ阿片受体以外的受体介导的。因此，如果强啡肽从感觉神经释放，可能在神经源性炎症中起作用。
