Burleigh D E, Kirkham S E
Department of Pharmacology, Queen Mary and Westfield College, London, UK.
Eur J Pharmacol. 1993 Nov 9;249(2):239-42. doi: 10.1016/0014-2999(93)90439-o.
We have assessed the potential usefulness of three vasoactive intestinal peptide antagonists for investigating whether vasoactive intestinal peptide has a functional role as a secretomotor neurotransmitter at the neuroepithelial junction in rat colonic mucosa. Vasoactive intestinal peptide (VIP) increases short-circuit current in muscle-stripped preparations of rat colon. The response is unaffected by tetrodotoxin and can only be obtained when the peptide is applied to the basolateral side of the membrane. Three putative antagonists were tested for their ability to inhibit short-circuit current responses to vasoactive intestinal peptide. Vasoactive intestinal peptide-(10-28) (1 microM and 3 microM), human growth hormone releasing factor (human GRF) analogue [Ac-Tyr1]human GRF-(1-40)OH (0.1 microM and 1 microM) and [Lys1,Pro2,5,Arg3,4,Tyr6]VIP (0.5 microM) produced concentration-dependent increases in basal short-circuit current but were ineffective as antagonists to vasoactive intestinal peptide.
我们评估了三种血管活性肠肽拮抗剂的潜在效用，以研究血管活性肠肽在大鼠结肠黏膜神经上皮连接处作为分泌运动神经递质是否具有功能性作用。血管活性肠肽（VIP）可增加大鼠结肠肌层剥离标本中的短路电流。该反应不受河豚毒素影响，且只有当该肽应用于膜的基底外侧时才能获得。测试了三种假定的拮抗剂抑制对血管活性肠肽的短路电流反应的能力。血管活性肠肽 -（10 - 28）（1微摩尔和3微摩尔）、人生长激素释放因子（人GRF）类似物[Ac - Tyr1]人GRF -（1 - 40）OH（0.1微摩尔和1微摩尔）以及[Lys1，Pro2，5，Arg3，4，Tyr6]VIP（0.5微摩尔）使基础短路电流呈浓度依赖性增加，但作为血管活性肠肽的拮抗剂无效。
