Ruoff H J, Sewing K F
Eur J Pharmacol. 1975 Jun-Jul;32(02):227-32. doi: 10.1016/0014-2999(75)90287-3.
In normal rats the effect of atropine and metiamide was studied on cAMP levels of resting and histamine-, pentagastrin-, carbachol- and insulin-stimulated gastric mucosa. In vagotomized rats gastric mucosal cAMP levels were investigated under basal conditions and after insulin. Atropine and metiamide did not alter cAMP levels of resting gastric mucosa. Truncal vagotomy caused an increase in gastric mucosal cAMP, which was not affected by insulin. All gastric secretagogues caused a significant rise in gastric mucosal cAMP levels, which was not antagonized by atropine. Metiamide effectively blocked the rise in cAMP concentration after histamine and pentagastrin, but not that evoked by cholinergic stimulation. The results are consistent with the view that the in vivo rise of gastric mucosal cAMP after carbachol or insulin is not due to a direct cholinergic action. From the spectrum of inhibitory actions of metiamide it looks as if the increase in rat gastric mucosal cAMP concentration after histamine and pentagastrin administration is mediated by H2-receptor stimulation.
在正常大鼠中,研究了阿托品和甲硫咪特对静息状态以及组胺、五肽胃泌素、卡巴胆碱和胰岛素刺激后的胃黏膜环磷酸腺苷(cAMP)水平的影响。在迷走神经切断的大鼠中,研究了基础状态下以及给予胰岛素后胃黏膜cAMP水平。阿托品和甲硫咪特未改变静息胃黏膜的cAMP水平。迷走神经干切断术导致胃黏膜cAMP升高,这不受胰岛素影响。所有胃促分泌剂均导致胃黏膜cAMP水平显著升高,且不受阿托品拮抗。甲硫咪特有效阻断了组胺和五肽胃泌素作用后cAMP浓度的升高,但未阻断胆碱能刺激引起的升高。这些结果与以下观点一致:卡巴胆碱或胰岛素作用后胃黏膜cAMP在体内升高并非由于直接的胆碱能作用。从甲硫咪特的抑制作用谱来看,组胺和五肽胃泌素给药后大鼠胃黏膜cAMP浓度的升高似乎是由H2受体刺激介导的。