SODIUM-DEPENDENT SECRETION AND RETENTION OF NE IN ADRENERGIC TERMINALS

钠离子依赖型高血压的发病机制及治疗效果 Li+是未知的。这份报告支持了钠调节的假设 肾上腺素能活动胺池中去甲肾上腺素的分泌和再捕获 大鼠心脏切片上的终末。锂产生一种功能性缺陷，即 娜。由于代谢的结果，动员的NE积累在终端 终端在通宵透析液中的缺陷 钠、钾、锂或胆碱在0度。轴膜是透析器 薄膜。在随后的孵化过程中，动员的NE被耗尽 终端在37度的克雷布斯介质(KRB)中。快速诱导的 消耗与一次透析阳离子无关，并且存在 KRB中的钙含量。无论是透析剂还是透析剂都能抑制衰竭。 (内部)三磷酸腺苷或可卡因等进口出口阻滞剂。这些特工 在孵育液中均未见抑制作用。移动网元的耗尽 不同于泡状NE的分泌。剩下的40% NE稳定地滞留在突触小泡中。小泡的分泌物 钠缺乏(胆碱)的KRB中终末的孵育引起的 (CH-Ca)。分泌延迟，依赖于肾小管内钠和钙。 灵媒。分泌是通过从前面描述的 囊泡-轴膜分泌和递质恢复单元，由 膜与轴膜融合的小泡。结合囊泡内 在这一过程中动员了NE，然后将其出口。囊泡膜为 在介质中可被ATP访问。在未透析的终末，分泌物是 只有在钠存在的情况下，才能被ATP抑制。因此，钠是必须的 去甲肾上腺素移入和移出终端。锂，在一种治疗方法中 浓度为1mM的ImM可防止囊泡重新捕获或释放。 动员型东北。这种作用表现为去甲肾上腺素脱氨基增加。 因此，李似乎干扰了在重新捕获时对Na的要求 活动单元中的进程。根据已公布的报告，李可能会采取行动 抑制分离突触的镁-三磷酸腺苷酶活性及对去甲肾上腺素的依赖摄取 水泡。本报告补充了李灿饰演的重要信息 在原位囊泡上的治疗浓度。既然李刺激了 在活体大鼠脑内去氨基作用，钠的假定作用可能是 在治疗上相关。

Mechanisms for both Na+-dependent hypertension and the therapeutic effect of Li+ are not known. This report supports the hypothesis that Na regulates the secretion and recapture of NE from a pool of mobile amine in adrenergic terminals in rat heart slices. Lithium produces a functional deficiency of Na. Mobilized NE was accumulated in terminals as a result of metabolic deficiencies during the overnight dialysis of terminals in solutions of either Na, K, Li or choline at 0 degrees. The axolemma was the dialysis membrane. The mobilized NE was depleted during a subsequent incubation of terminals in Krebs medium (KRB) at 37 degrees. The rapidly induced depletion was independent of the primary dialysis cation, and, the presence of Ca in the KRB. Depletion was inhibited by either dialyzed (intraterminal) ATP or import export blockers such as cocaine. These agents in the incubation medium were not inhibitory. The depletion of mobile NE differed from the secretion of vesicular NE. Forty percent of the remaining NE was stably retained in synaptic vesicles. Secretion from vesicles was evoked by the incubation of terminals in a Na-deprived (Choline) KRB (Ch-Ca). Secretion was delayed, dependent upon intraterminal Na, and, Ca in the medium. Secretion was mediated by export from a previously described vesicular-axolemmal secretory and transmitter recovery unit comprised of vesicles whose membranes had fused with the axolemma. Bound intravesicular NE was mobilized in the process then exported. The vesicle membrane was accessible to ATP in the medium. In non-dialyzed terminals, secretion was inhibited by ATP only when Na was present. Thus, Na was required for the translocation of NE into and out of terminals. Lithium, in a therapeutic concentration of I mM prevented the vesicle from recapturing released or mobilized NE. This effect was indicated by an increased deamination of NE. Thus, Li appeared to interfere with a requirement for Na in the recapture process in an active unit. On the basis of published reports, Li may act by inhibiting Mg-ATPase activity and dependent NE uptake in isolated synaptic vesicles. The present report adds the important information that Li can act in therapeutic concentrations on vesicles in situ. Since Li stimulates deamination in rat brain in vivo, the postulated role for Na may be relevant therapeutically.