MECHANISMS OF UPTAKE OF NOREPINEPHRINE IN ADRENERGIC STORAGE VESICLES IN SITU

生物化学证据已被引证来支持这一假设， 肾上腺素能神经分泌可通过以下物质的向外转运来介导： 去甲肾上腺素（NE）来自突触囊泡，其融合或附着于 神经末梢的质膜 此外，吸收理论和 在蔗糖基培养基中孵育的分离囊泡对NE的保留似乎 通过我们的实验来验证， 离体心室片的神经末梢。 结果提示 囊泡摄取和保留NE的驱动力是 通过Mg-ATPase的活性建立H+的电化学梯度。 然而，Mg-ATP酶活性的这些原位效应发生在存在 高浓度的C1- 在蔗糖中孵育的孤立囊泡中 与ATP一起，C1-抑制摄取并诱导囊泡溶解。 的摄取 NE通过囊泡原位被Li+、N-乙基马来酰亚胺（NEM）和 二环己基碳二亚胺（DCCD），它们都是Mg-ATPase的抑制剂。 2，4-二硝基苯酚（2，4-DNP）是一种H+的还原剂，它也能抑制细胞的吸收 电化学梯度，（NH 4）2SO 4，其中和建立的pH 梯度穿过囊泡膜，和尼日利亚菌素，这有助于 H+和K+跨膜的电中性交换。 显然，非胞吐分泌可在存在 生理浓度的C1-。

Biochemical evidence has been adduced to support the hypothesis that adrenergic neurosecretion can be mediated by the outward transport of norepinephrine (NE) from synaptic vesicles that are fused or attached to the plasma membrane of the nerve ending. Moreover, theories of uptake and retention of NE by isolated vesicles incubated in sucrose-based media seem to be verified by our experiments in which the vesicles are located within the nerve endings in heart ventricle slices in vitro. The results suggest that a driving force for the uptake and retention of NE by vesicles is the electro-chemical gradient of H+ established by the activity of Mg-ATPase. However, these effects of Mg-ATPase activity in situ occur in the presence of high concentrations of C1-. In isolated vesicles incubated in sucrose with ATP, C1-inhibits uptake and induces lysis of vesicles. The uptake of NE by vesicles in situ is blocked by Li+, N-ethylmaleimide (NEM), and Dicyclohexylcarbodiimide (DCCD) which are all inhibitors of Mg-ATPase. Uptake is also inhibited by 2,4-dinitrophenol (2,4-DNP) a dissipator of H+ electrochemical gradients, (NH4)2S04 which neutralizes an established pH gradient across the vesicle membrane, and nigericin, which facilitates an electrically neutral exchange of H+ and K+ across the membrane. Apparently, non-exocytotic secretion can occur in the presence of physiological concentrations of C1-.