Fujimiya M, Yamamoto H, Kuwahara A
Department of Anatomy, Shiga University of Medical Science, Japan.
Ann N Y Acad Sci. 1998 Dec 11;865:495-502. doi: 10.1111/j.1749-6632.1998.tb11224.x.
Effects of CCK, VIP, PACAP38, and PACAP27 on the release of 5HT into the intestinal lumen and into the portal circulation were examined in in vivo experiments of isolated rat duodenum perfused vascularly and luminally. VIP, PACAP 38 and 27 reduced the release of 5HT into the lumen but did not affect the vascular release of 5HT. These effects were not affected by the presence of atropine, hexamethonium, or TTX, suggesting that VIP, PACAP 38 and 27 exert a direct inhibitory effect on the luminal release of 5HT from the EC cells. Nitric oxide synthase inhibitor, NG-nitro-L-arginine, antagonized the inhibitory effects of VIP, PACAP 38 and 27, suggesting that nitric oxide seems to be essential to exert the inhibitory action of VIP and PACAPs on the release of 5HT into the intestinal lumen from the EC cells.
在大鼠离体十二指肠进行血管内和管腔内灌注的体内实验中,研究了胆囊收缩素(CCK)、血管活性肠肽(VIP)、38 肽垂体腺苷酸环化酶激活肽(PACAP38)和 27 肽垂体腺苷酸环化酶激活肽(PACAP27)对 5-羟色胺(5HT)释放到肠腔和门静脉循环中的影响。VIP、PACAP38 和 PACAP27 减少了 5HT 向肠腔内的释放,但不影响 5HT 的血管性释放。这些效应不受阿托品、六甲铵或河豚毒素(TTX)的影响,表明 VIP、PACAP38 和 PACAP27 对肠嗜铬(EC)细胞向肠腔内释放 5HT 具有直接抑制作用。一氧化氮合酶抑制剂 NG-硝基-L-精氨酸拮抗了 VIP、PACAP38 和 PACAP27 的抑制作用,表明一氧化氮似乎对于 VIP 和 PACAP 对 EC 细胞向肠腔内释放 5HT 的抑制作用至关重要。