首页> 外文期刊>Japanese Journal of Pharmacology >Effects of Adenylate Cyclase Inhibitors, Phosphodiesterase Inhibitors, and Dibutyryl Cyclic AMP on Spontaneous and Various Stimuli-Induced Acetylcholine Release from Guinea Pig Ileum Myenteric Plexus
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Effects of Adenylate Cyclase Inhibitors, Phosphodiesterase Inhibitors, and Dibutyryl Cyclic AMP on Spontaneous and Various Stimuli-Induced Acetylcholine Release from Guinea Pig Ileum Myenteric Plexus

机译:腺苷酸环化酶抑制剂,磷酸二酯酶抑制剂和二丁酰环AMP对豚鼠回肠肌间盘丛自发释放和各种刺激诱导的乙酰胆碱释放的影响

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References(27) Cited-By(7) In order to examine a possible contribution of cyclic AMP to acetylcholine (ACh) release from guinea pig ileum myenteric plexus, effects of adenylate cyclase inhibitors, phosphodiesterase (PDE) inhibitors and dibutyryl cyclic AMP on the spontaneous and the various stimuli-induced ACh release were investigated. A PDE inhibitor, theophylline (1 mM) increased the ACh release induced by nicotine (6.16 μM) significantly. Another PDE inhibitor, 3-isobutyl-1-methylxanthine (IBMX, 1 mM) and dibutyryl cyclic AMP (4 mM) had no effect. The adenylate cyclase inhibitors dithiobisnitrobenzoic acid (DTNB, 1 mM) and alloxan (4 mM) both decreased the nicotine-induced ACh release remarkably. PDE inhibitors increased and adenylate cyclase inhibitors decreased the high-K+-induced ACh release. Dibutyryl cyclic AMP brought about a slight but significant increase of the high-K+-induced ACh release. All the drugs failed to alter the ACh release induced by electrical field stimulation (EFS) at 10 Hz. Effects of all drugs except dibutyryl cyclic AMP on the spontaneous ACh release were the same as those on the nicotine-induced one. Dibutyryl cyclic AMP decreased it significantly. These results suggest that the cyclic AMP system is involved in the spontaneous, the nicotine-induced and the high-K+-induced ACh release and that the EFS-induced ACh release is independent of cyclic AMP.
机译:参考文献(27)Cited-By(7)为了检查环状AMP对豚鼠回肠肌层神经丛乙酰胆碱(ACh)释放的可能贡献,腺苷酸环化酶抑制剂,磷酸二酯酶(PDE)抑制剂和二丁酰基环状AMP对研究了自发性和各种刺激诱导的乙酰胆碱释放。 PDE抑制剂茶碱(1 mM)显着增加了尼古丁(6.16μM)诱导的ACh释放。另一种PDE抑制剂3-异丁基-1-甲基黄嘌呤(IBMX,1 mM)和二丁酰基环AMP(4 mM)无效。腺苷酸环化酶抑制剂二硫代双硝基苯甲酸(DTNB,1 mM)和四氧嘧啶(4 mM)均显着降低了尼古丁诱导的ACh释放。 PDE抑制剂增加,腺苷酸环化酶抑制剂减少高K +诱导的ACh释放。二丁酰环AMP导致高K +诱导的ACh释放略有但显着增加。所有药物均未改变10 Hz电场刺激(EFS)诱导的ACh释放。除二丁酰基环AMP以外的所有药物对自发性ACh释放的影响与对尼古丁诱导的药物的影响相同。二丁酰基环AMP显着降低了它。这些结果表明,环状AMP系统参与自发的,尼古丁诱导的和高K +诱导的ACh的释放,而EFS诱导的ACh的释放与环状AMP无关。

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