Black J W, Shankley N P
Br J Pharmacol. 1986 May;88(1):291-7. doi: 10.1111/j.1476-5381.1986.tb09498.x.
The muscarinic receptors involved in the vagal stimulation of gastric acid secretion in the mouse isolated stomach assay have been examined by analysing the effects of pirenzepine and atropine on fully-defined frequency-effect curves. Both atropine and pirenzepine produced concentration-dependent inhibition of vagal-stimulated acid secretion in a manner consistent with a model describing competitive antagonism of endogenous acetylcholine, which was assumed to be released by vagal stimulation. The results obtained are quite compatible with the hypothesis that vagal stimulation involves muscarinic receptors which are homogeneous with those previously found on histamine and oxyntic cells in the mouse stomach assay. These results find no evidence for muscarinic receptor heterogeneity and reinforce the hypothesis that the selectivity of pirenzepine in vivo relative to atropine is due to the loss of atropine into the gastric secretion.
通过分析哌仑西平和阿托品对完全确定的频率-效应曲线的影响，研究了在小鼠离体胃实验中参与迷走神经刺激胃酸分泌的毒蕈碱受体。阿托品和哌仑西平均以与描述内源性乙酰胆碱竞争性拮抗作用的模型相一致的方式，产生浓度依赖性抑制迷走神经刺激的胃酸分泌，内源性乙酰胆碱假定是由迷走神经刺激释放的。所得结果与下述假设完全相符，即迷走神经刺激涉及的毒蕈碱受体与先前在小鼠胃实验中组胺细胞和壁细胞上发现的受体是同质的。这些结果没有发现毒蕈碱受体异质性的证据，并强化了下述假设，即哌仑西平在体内相对于阿托品的选择性是由于阿托品进入胃分泌中所致。
