Coupling between platelet 5-hydroxytryptamine and potassium transport.
Coupling between platelet 5-hydroxytryptamine and potassium transport.
复制标题
血小板 5-羟色胺和钾转运之间的偶联。
DOI：
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发表时间：
1979
影响因子：
4.8
通讯作者：
G. Rudnick
中科院分区：
文献类型：
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作者：
P. J. Nelson;G. Rudnick
血小板质膜囊泡对NaCl浓度梯度（out > in）的反应是积累5-羟色胺.虽然该过程不需要钾离子，但K'浓度梯度（输入>输出）使5-羟色胺累积的稳态水平提高5倍。当K'存在于囊泡内部时，转运与跨囊泡膜的电位（内部负）的产生无关，但在K'不存在的情况下，5-羟色胺转运显然是产电的，净正电荷与5-羟色胺一起跨膜。钾离子直接与5-羟色胺转运体相互作用，这可通过其对5-羟色胺转运初始速率的影响来证明。内部K+刺激流入，外部K'抑制。即使在没有K ′梯度的情况下，K ′也影响5-羟色胺转运的动力学，30 meq/L的K ′使5-羟色胺转运的Vmin增加3倍，Kmin增加2倍。[~ 3 H]5-羟色胺的单向外排可被K'和未标记的5-羟色胺所刺激。虽然5-羟色胺刺激的外排需要外部Na+，但K '诱导的外排不依赖于外部Na'。提出了与上述观察一致的一种机制，即内部K+通过增加转运体的5-羟色胺结合位点从质膜内表面“移动”到外表面的速率来加速5-羟色胺的内流。伴随着这种运动，一个钾离子从囊泡腔运输到外部介质。血小板蓄积5-羟色胺的过程被认为与肾上腺素能神经元对5-羟色胺的再摄取相似（如果不完全相同）（1，2）。在这两种情况下，转运都是能量依赖性载体介导的过程，绝对需要外部介质中的Na'和Cl-（3-10）。从血小板中分离的质膜囊泡提供了一个有用的模型系统，
Platelet plasma membrane vesicles accumulate 5-hy- droxytryptamine in response to a gradient of NaCl (out > in). Although potassium ion is not required for this process, a K’ concentration gradient (in > out) elevates the steady state level of 5-hydroxytryptamine accu- mulation 5-fold. Transport is independent of the gen- eration of an electrical potential (interior negative) across the vesicle membrane when K’ is present inter- nally, but in its absence 5-hydroxytryptamine trans- port is apparently electrogenic, with net positive charge crossing the membrane with 5-hydroxytrypt- amine. Potassium ion directly interacts with the 5-hy- droxytryptamine transporter as evidenced by its ef- fects on the initial rate of 5-hydroxytryptamine trans- port. Internal K+ stimulates influx and external K’ inhibits. Even in the absence of a K’ gradient, K’ affects the kinetics of 5-hydroxytryptamine transport, 30 meq of K’/liter increasing the V,,,,, for 5-hydroxy- tryptamine transport 3-fold and increasing K,,, by 2- fold. The unidirectional efflux of [3H]5-hydroxytrypt- amine is stimulated by both K’ and unlabeled 5-hy- droxytryptamine in the external medium. Although 5- hydroxytryptamine-stimulated efflux requires external Na+, K’-induced efflux is independent of external Na’. A mechanism consistent with the above observations is proposed in which internal K+ accelerates the influx of 5-hydroxytryptamine by increasing the rate at which the 5-hydroxytryptamine binding site of the trans- porter “moves” from the internal surface of the mem- brane to the external surface. Concomitant with this movement, one potassium ion is transported from the vesicle lumen to the external medium. Blood platelets accumulate 5-hydroxytryptamine by a proc- ess which is believed to be similar, if not identical, to the reuptake of Shydroxytryptamine by serotonergic neurons (1, 2). In both cases, transport is an energy-dependent carrier- mediated process with an absolute requirement for Na’ and Cl- in the external medium (3-10). Plasma membrane vesicles isolated from platelets provide a useful model system for the