MECHANISMS OF UPTAKE AND RELEASE OF NOREPINEPHRINE IN ADRENERGIC NERVE ENDINGS

越来越多的证据继续支持我们的假设， 肾上腺素能神经末梢介导Ch+-Ca++刺激的神经分泌 通过NE在融合或附着于细胞膜的囊泡中的向外运输 质膜 总体计划是并且一直是诱导Ca++依赖性 大鼠心室片在去Na+培养液中的神经分泌 含有氯化胆碱的克雷布斯碳酸氢盐培养基作为 氯化钠。 质膜的完整性由Ca++依赖性， K+诱导的分泌后，用适当的 修改实验条件。 囊泡的生化证据 融合是已知的表征囊泡的反应的示范。 膜。 通过不可渗透的ATP抑制分泌是这样的一种方法， 反应 根据浓度，氯丙嗪，一种已知的药物 对生物膜有多种作用，抑制H+ 转运，可增加或减少Ch+-Ca++刺激的神经分泌。 育亨宾对特异性α受体阻断作用不大 浓度的 建立的分泌是可逆的， 细胞外Ca++。

Accumulating evidence continues to be supportive of our hypothesis that Ch+-Ca++-stimulated neurosecreton by adrenergic nerve endings is mediated by outward transport of NE in vesicles fused or attached to the plasmalemma. The overall plan is and has been to induce Ca++ dependent neurosecretion by rat heart ventricle slices incubated in a Na+ deprived Krebs bicarbonate medium containing choline Cl as the replacement for NaCl. The integrity of the plasmalemma was shown by a Ca++-dependent, secretion induced by K+ after secretion was slowed by appropriate modification of experimental conditions. Biochemical evidence of vesicles fusion was the demonstration of reactions known to characterize vesicle membranes. Inhibition of secretion by the impermeable ATP is such a reaction. Depending upon the concentration, chlorpromazine, a drug known to have a variety of effects on biological membranes, and to inhibit H+ transport, may increase or decrease Ch+-Ca++ stimulated neurosecretion. Yohimbine had little effect in specific alpha receptor blocking concentrations. Established secretion was reversible by the ommission of extracellular Ca++.