Koop H, Behrens I, Bothe E, McIntosh C H, Pederson R A, Arnold R, Creutzfeldt W
Digestion. 1982;25(2):96-102. doi: 10.1159/000198817.
The interactions of adrenergic and cholinergic influences on the gastric D cell were studied using an isolated perfused rat stomach in vitro. The sevenfold increase in the release of somatostatin-like immunoreactivity (SLI) in response to isoproterenol (4 . 10(-8) M) was dose-dependently inhibited by acetylcholine (10(-5) to 10(-8) M) whereas gastrin levels increased in a dose-dependent manner. Both inhibition of stimulated SLI and augmentation of gastrin release were completely abolished by atropine (10(-6) M). Isoproterenol (8 . 10(-9) M)-induced stimulation of SLI secretion was not altered by atropine. Antral exclusion completely eliminated gastrin secretion but basal and beta-adrenergic stimulated SLI release was not influenced. It is concluded that (1) cholinergic agonism reverses the stimulatory action of adrenergic agonists on the D cell, and (2) SLI from the rat stomach in vitro originates almost exclusively in the fundic region.
利用离体灌注大鼠胃，研究了肾上腺素能和胆碱能对胃D细胞的相互作用。异丙肾上腺素（4×10⁻⁸ M）使生长抑素样免疫反应性（SLI）释放增加7倍，该效应呈剂量依赖性地被乙酰胆碱（10⁻⁵至10⁻⁸ M）抑制，而胃泌素水平则呈剂量依赖性升高。阿托品（10⁻⁶ M）可完全消除对刺激的SLI的抑制以及胃泌素释放的增强。阿托品不改变异丙肾上腺素（8×10⁻⁹ M）诱导的SLI分泌刺激。胃窦切除完全消除了胃泌素分泌，但基础和β-肾上腺素能刺激的SLI释放不受影响。得出的结论是：（1）胆碱能激动作用可逆转肾上腺素能激动剂对D细胞的刺激作用；（2）体外大鼠胃中的SLI几乎完全起源于胃底区域。
