Wessler I, Hellwig D, Racké K
Pharmakologisches Institut, Universität Mainz, Federal Republic of Germany.
Naunyn Schmiedebergs Arch Pharmacol. 1990 Oct;342(4):387-93. doi: 10.1007/BF00169454.
To investigate presynaptic, regulatory mechanisms on parasympathetic nerve fibres innervating the airways, the release of newly-synthesized [3H]acetylcholine from the isolated trachea was studied. Reverse phase HPLC followed by liquid scintillation spectrometry was used to separate and quantify the radioactive compounds choline, phosphorylcholine and acetylcholine in the incubation medium and the tissue. During the incubation of the tracheae with [3H]choline a significant synthesis of [3H]acetylcholine (35,000 dpm/preparation) and [3H]phosphorylcholine (500,000 dpm/preparation) occurred. In epithelium-deficient tracheae the formation of [3H]phosphorylcholine was enhanced, whereas the content of [3H]acetylcholine remained unchanged. The spontaneous outflow of tritium consisted mainly of [3H]phosphorylcholine (900 dpm/3 min) and [3H]choline (800 dpm/3 min); [3H]acetylcholine was only a minor fraction (50 dpm/3 min). Electrical stimulation of tracheae with intact epithelium caused only a small release of [3H]acetylcholine (460 dpm in the sample obtained during stimulation), but a considerable outflow of [3H]phosphorylcholine (1,900 dpm) without affecting the outflow of [3H]choline. Electrical stimulation of epithelium-deficient tracheae, however, induced a substantial release of [3H]acetylcholine (2,400 dpm), but only a small outflow of [3H]phosphorylcholine. Chemical stimulation (30 mumol/l veratridine) also caused a large release of [3H]acetylcholine (1,700 dpm) without affecting the outflow of [3H]phosphorylcholine or [3H]choline. Indomethacin (3 mumol/l) enhanced the electrically-evoked release of [3H]acetylcholine from tracheae with intact epithelium by 89%. The present experiments demonstrate a strong inhibition by the epithelium of the electrically-evoked release of [3H]acetylcholine from the isolated guinea-pig trachea. Cyclooxygenase products of arachidonic acid do not appear as the main mediators of the epithelium-derived inhibition of acetylcholine release.
为研究支配气道的副交感神经纤维的突触前调节机制，对分离出的气管中新合成的[3H]乙酰胆碱的释放进行了研究。采用反相高效液相色谱法，随后进行液体闪烁光谱法，以分离和定量孵育培养基及组织中的放射性化合物胆碱、磷酸胆碱和乙酰胆碱。在用[3H]胆碱孵育气管的过程中，显著合成了[3H]乙酰胆碱（35,000 dpm/制剂）和[3H]磷酸胆碱（500,000 dpm/制剂）。在缺乏上皮的气管中，[3H]磷酸胆碱的形成增强，而[3H]乙酰胆碱的含量保持不变。氚的自发流出主要由[3H]磷酸胆碱（900 dpm/3分钟）和[3H]胆碱（800 dpm/3分钟）组成；[3H]乙酰胆碱只是一小部分（50 dpm/3分钟）。对具有完整上皮的气管进行电刺激，仅引起少量[3H]乙酰胆碱的释放（刺激期间获得的样品中为460 dpm），但有相当数量的[3H]磷酸胆碱流出（1,900 dpm），而不影响[3H]胆碱的流出。然而，对缺乏上皮的气管进行电刺激，会诱导大量[3H]乙酰胆碱的释放（2,400 dpm），但只有少量[3H]磷酸胆碱流出。化学刺激（30 μmol/L藜芦碱）也会引起大量[3H]乙酰胆碱的释放（1,700 dpm），而不影响[3H]磷酸胆碱或[3H]胆碱的流出。吲哚美辛（3 μmol/L）使具有完整上皮的气管中电诱发的[3H]乙酰胆碱释放增加了89%。本实验表明，上皮对分离的豚鼠气管中电诱发的[3H]乙酰胆碱释放有强烈抑制作用。花生四烯酸的环氧化酶产物似乎不是上皮来源的乙酰胆碱释放抑制作用的主要介质。
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