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用荧光素－荧光素酶方法测定大鼠盆总神经节腺苷三磷酸（ＡＴＰ）释放．钠通道阻断剂河豚毒素（１μｍｏｌ·Ｌ－１）抑制电刺激诱发的盆总神经节ＡＴＰ的释放．灌流液中去除Ｃａ２＋并加入ＥＧＴＡ（１ｍｍｏｌ·Ｌ－１）后消除ＡＴＰ的释放．腺苷（１００μｍｏｌ·Ｌ－１），Ａ１腺苷受体激动剂环戊腺苷（０．１μｍｏｌ·Ｌ－１），毒蕈碱性受体激动剂氧化震颤素（１μｍｏｌ·Ｌ－１）和５－羟色胺（１００μｍｏｌ·Ｌ－１）减少ＡＴＰ的释放．Ａ１腺苷受体拮抗剂８－环戊基－１，３－二丙基黄嘌呤（１０ｎｍｏｌ·Ｌ－１），α２肾上腺素受体拮抗剂育亨宾（３μｍｏｌ·Ｌ－１），Ｄ２多巴胺受体拮抗剂舒必利（２０μｍｏｌ·Ｌ－１）和组胺（１００μｍｏｌ·Ｌ－１）增加ＡＴＰ的释放．结果提示，在大鼠盆总神经节存在着作为神经递质参与突触传递的ＡＴＰ释放．Ａ１腺苷受体，毒蕈碱性受体，α２肾上腺素受体，Ｄ２多巴胺受体，５－羟色胺受体及Ｈ１组胺受体激动剂或拮抗剂可以通过节前机制影响ＡＴＰ的释放
The release of adenosine triphosphate (ATP) in the pelvic ganglion of rats was measured by fluorescein - luciferase method. Tetrodotoxin (1μmol·L-1), a sodium channel blocker, inhibited the release of ATP from pelvic ganglion neurons induced by electrical stimulation. Removal of Ca2 + in the perfusate and the addition of EGTA (1 mmol·L-1) abolished the release of ATP. Adenosine (100μmol·L-1), A1 adenosine receptor agonist cyclopendenosine (0.1μmol·L-1), muscarinic receptor agonist oxotremorine (1μmol·L-1) and Serotonin (100 μmol·L-1) reduced ATP release. A1 adenosine receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (10nmol·L-1), α2-adrenoceptor antagonist yohimbe (3μmol·L-1), D2 dopamine Receptor antagonists sulpiride (20μmol·L-1) and histamine (100μmol·L-1) increased ATP release. The results suggest that there is ATP release involved in synaptic transmission as a neurotransmitter in the rat gullet. A1 adenosine receptors, muscarinic receptors, α2 adrenoceptors, D2 dopamine receptors, serotonin receptors, and H1 histamine receptor agonists or antagonists may affect the release of ATP via an anterior preganglionic mechanism