Substance P and bradykinin stimulate plasma extravasation in the mouse gastrointestinal tract and pancreas
Substance P and bradykinin stimulate plasma extravasation in the mouse gastrointestinal tract and pancreas
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DOI：
10.1152/ajpgi.1997.272.4.g785
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发表时间：
1997-04-01
影响因子：
4.5
通讯作者：
Bunnett, N
中科院分区：
文献类型：
--
作者：
Figini, M;Emanueli, C;Bunnett, N
神经源性炎症由感觉神经释放速激肽介导，其刺激毛细血管后微静脉的血浆外渗。由于在胃肠道神经源性炎症的重要性方面存在相互矛盾的结果，我们使用Evans蓝定量血浆外渗，并使用Monastral蓝在小鼠中鉴定渗漏部位。P物质和缓激肽通过分别与NK 1和B-2受体相互作用，刺激胃、小肠和大肠、胰腺、膀胱、气管和皮肤毛细血管后微静脉外渗2 - 7倍。辣椒素刺激感觉神经也会引起外渗。辣椒素和缓激肽刺激的外渗减弱的NK 1受体拮抗剂，因此介导的释放速激肽和激活的NK 1受体。我们的结论是：1）P物质通过与NK 1受体相互作用刺激小鼠胃肠道和胰腺外渗，2）辣椒素和缓激肽通过刺激感觉神经释放速激肽诱导血浆外渗。因此，神经原性机制介导小鼠胃肠道和胰腺中的炎症。
Neurogenic inflammation is mediated by release of tachykinins from sensory nerves, which stimulate plasma extravasation from postcapillary venules. Because there are conflicting results regarding the importance of neurogenic inflammation in the gastrointestinal tract, we quantified plasma extravasation using Evans blue and identified sites of the leak using Monastral blue in the mouse. Substance P and bradykinin stimulated extravasation from postcapillary venules in the stomach, small and large intestine, pancreas, urinary bladder, trachea, and skin by two- to sevenfold by interacting with NK1 and B-2 receptors, respectively. Stimulation of sensory nerves with capsaicin also induced extravasation. Capsaicin- and bradykinin-stimulated extravasation was attenuated by an NK1-receptor antagonist and is thus mediated by release of tachykinins and activation of the NK1 receptor. We conclude that 1) substance P stimulates extravasation in the gastrointestinal tract and pancreas of mice by interacting with the NK1 receptors, and 2) capsaicin and bradykinin induce plasma extravasation by stimulating tachykinin release from sensory nerves. Thus neurogenic mechanisms mediate inflammation in the gastrointestinal tract and pancreas of the mouse.