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Releasing mechanisms of acetylcholine from an isolated rat stomach

离体大鼠胃中乙酰胆碱的释放机制

基本信息

批准号：
04671416
负责人：
YOKOTANI Kunihiko
金额：
$ 1.41万
依托单位：
Kochi Medical School
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1992
资助国家：
日本
起止时间：
1992 至 1993
项目状态：
已结题

项目摘要

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.

用改良的Krebs-Ringer液测定了离体大鼠胃血管灌流时内源性乙酰胆碱（ACh）和去甲肾上腺素（NA）的溢出。用酶反应和/或高效液相色谱电化学测定释放到灌流液中的ACh和NA。2.5Hz刺激迷走神经诱发的ACh溢出可被毒蕈碱激动剂氧震颤素抑制，阿托品、M_3受体拮抗剂4-DAMP、M_2受体拮抗剂甲氧曲明和M_1受体拮抗剂哌仑西平增强，其作用强弱顺序为阿托品> 4-DAMP >甲氧曲明>哌仑西平。α 2肾上腺素能受体激动剂可乐定浓度依赖性地减少诱发的ACh溢出，电刺激动脉周围胃交感神经（5 Hz）也抑制诱发的ACh溢出。这种对ACh溢出的交感神经抑制作用可被α 2肾上腺素能受体拮抗剂萝芙木碱（rauwolscine）所消除，但不能被α 1肾上腺素能受体拮抗剂哌唑嗪（prazosin）所消除。电刺激含有胃交感神经的动脉周围神经诱发频率依赖性NA溢出。双侧迷走神经刺激（5 Hz）或oxotremorine抑制诱发的NA溢出。阿托品<-7>、甲氧曲明、4-DAMP和哌仑西平均能减弱氧震颤素（10 μ M）对NA溢出的抑制作用，其强度依次为阿托品>甲氧曲明> 4-DAMP >哌仑西平。上述结果表明，激活M_2受体可抑制胃交感神经末梢释放NA，激活M_3受体和α_2受体可抑制胃迷走神经末梢释放ACh。在胃壁中，交感神经系统和副交感神经系统之间的相互作用可能在胃功能的调节中起重要作用。