Releasing mechanisms of acetylcholine from an isolated rat stomach

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We measured endogenous acetylcholine (ACh) and noradrenaline (NA) overflow from a vascularly perfused rat stomach in vitro with modified Krebs-Ringer solution. ACh and NA released into the perfusate were electrochemically measured with enzyme reaction and/or high performance liquid chromatography. Evoked ACh overflow by vagal stimulation at 2.5 Hz was inhibited by oxotremorine (muscarinic agonist) and enhanced by atropine, 4-DAMP(M3 receptor antagonist), methoctramine(M2 receptor antagonist) and pirenzepine(M1 receptor antagonist) with the following potency ; atropine > 4-DAMP > methoctramine > pirenzepine. Clonidine (alpha-2 adrenoceptor agonist) concentration-dependently decreased the evoked ACh overflow and electrical stimulation of periarterial gastric sympathetic nerves (5 Hz) also inhibited the evoked ACh overflow. This sympathetic inhibition of ACh overflow was abolished by rauwolscine (alpha-2 adrenoceptor antagonist), but not by prazosin (alpha-1 adrenoceptor antagonist). Electrical stimulation of periarterial nerves containing gastric sympathetic nerves evoked frequency-dependent NA overflow. Bilateral vagus nerve stimulation (5 Hz) or oxotremorine inhibited evoked NA overflow. Oxotremorine (l0^<-7> M)-induced inhibition of NA overflow was attenuated by atropine, methoctramine , 4-DAMP and pirenzepine with the following potency ; atropine > methoctramine > 4-DAMP >> pirenzepine. These results indicate that NA release from gastric sympathetic nerve terminals is inhibited by activation of muscarinic M_2 receptor and that ACh release from gastric vagal nerves is inhibited by M_3 muscarinic autoreceptors and alpha-2 adrenoceptors. In the gastric wall, interaction between sympathetic and parasympathetic nervous systems may play an important role in regulation of gastric functions.