Kan S, Niwa M, Taniyama K
Department of Pharmacology II, Nagasaki University School of Medicine, Japan.
Eur J Pharmacol. 1994 Jun 2;258(1-2):139-43. doi: 10.1016/0014-2999(94)90066-3.
The receptor for vasoactive intestinal contractor (VIC) involved in acetylcholine release was examined in the guinea-pig ileum. VIC (10(-9) to 10(-7) M) evoked tritium outflow from ileal strips preloaded with [3H]choline, in a concentration-dependent manner. The evoked tritium outflow was Ca(2+)-dependent and tetrodotoxin-sensitive, suggesting that VIC acts on somato-dendritic regions of the cholinergic neurones to stimulate acetylcholine release. The response to VIC did not change after desensitization to either endothelin-1, endothelin-2 or endothelin-3, hence there is probably no cross-desensitization in evoked tritium outflow between VIC and endothelins. VIC-induced contractions consisted of tetrodotoxin-sensitive and -resistant contractions, and the tetrodotoxin-resistant contraction was abolished after desensitization to either endothelin-1, endothelin-2 or endothelin-3. These results indicate that the VIC-specific receptor is located on cholinergic neurones, but not on the smooth muscle cells of guinea-pig ileum.
在豚鼠回肠中研究了参与乙酰胆碱释放的血管活性肠收缩因子（VIC）的受体。VIC（10^(-9)至10^(-7)M）以浓度依赖性方式引起预先加载[3H]胆碱的回肠条带中的氚流出。诱发的氚流出是钙依赖性的且对河豚毒素敏感，表明VIC作用于胆碱能神经元的体树突区域以刺激乙酰胆碱释放。对VIC的反应在对内皮素-1、内皮素-2或内皮素-3脱敏后没有改变，因此在VIC和内皮素诱发的氚流出之间可能不存在交叉脱敏。VIC诱导的收缩由对河豚毒素敏感和不敏感的收缩组成，并且在对内皮素-1、内皮素-2或内皮素-3脱敏后，对河豚毒素不敏感的收缩被消除。这些结果表明，VIC特异性受体位于胆碱能神经元上，而不在豚鼠回肠的平滑肌细胞上。
