Novel characteristics of ATP as a potential neuro-co-transmitter.

近年来的研究表明，ATP在肾上腺素能优势组织中与经典递质去甲肾上腺素（NA）一起作为沿着神经共递质发挥作用。1986 ~ 1987年的研究旨在进一步阐明NA和ATP在豚鼠输精管中的共传递特征。第一年的HPLC-ECD研究表明，哇巴因（100<micrn>）和（或）莫能菌素（10<micrn>），但高KCl，产生了颗粒状NA的显著释放，这是由细胞内Ca^2+介导的，据推测，除了测量这种NA释放外，1987年的研究是在存在促分泌剂如哇巴因加莫能菌素和高KCl的情况下通过发光计数法测量从组织释放的ATP。6-羟基多巴胺和哌唑嗪均能显著降低ATP的释放，因此，这主要意味着神经元释放核苷酸。另一方面，高KCl引起的ATP释放被6-羟基多巴胺或Ca^2+去除显著降低，但哌唑嗪不降低，这主要表明神经元释放ATP。哇巴因加莫能菌素和高KCl引起的神经元释放ATP的量分别为1.7 <micrn>g和11.2 <micrn>g/g湿重。另一方面，相同程序引起的神经元释放NA的量分别为7.7 <micrn>g和1.7 <micrn>g/g湿重。这些结果有力地支持了这样一种可能性，即NA和ATP是通过去极化和细胞内Na^+水平升高从肾上腺素能神经的两个不同储存部位共同释放的。

Recent findings provide evidence that ATP is capable of acting as a neuro-co-transmitter along with the classical transmitter,noradrenaline(NA)in adrenergically dominant tissues.The research project from 1986 to 1987 was designed to clarify further characteristics of cotransmission of NA and ATP from guinea-pig vas deferens.The study with HPLC-ECD in the first year disignated that ouabain(100<micrn>and/or monesin(10<micrn>),but not high KCI,produced a prominent liberation of granular NA which was mediated by intracellular Ca^<2+> originating, presumably,from mitochondrial store sites.In addition to measuring this NA release.the investigation in 1987 was to measure ATP released from the tissue by a lumicounting method in the presence of secretagogues such as ouabain plus monensin and high KCI.Ouabain plus monensin caused a moderate outflow of atp which was markedly diminished by both 6-hydroxydopamine and prazosin,thus,meaning primarily an extraneuronal release of the nucleotide.On the other hand,an outstanding liberation of ATP by high KCI was highly decreased by 6-hydroxydopamine or Ca^<2+>-removal,but not by prazosin,indicating,mainly a neuronal ATP release.Amounts of neuronal release of ATP by ouabain plus monensin and by high KCl were 1.7<micrn>g and 11.2<micrn>g/g wet weight,respectively.On the other hand,that of neuronal release of NA by the same procedures amounted to 7.7<micrn>g and 1.7<micrn>g/g wet weight,respectively.These results strongly support a possibility that NA and ATP are co-released from two different store sites of the adrenergic nerves by depolarization and elevation of intracellular Na^+ levels.