Ruifrok P G, Meijer D K
Liver. 1982 Mar;2(1):28-34. doi: 10.1111/j.1600-0676.1982.tb00175.x.
Uptake of taurocholate into plasma membrane vesicles isolated from rat liver was investigated. In the presence of an extra- to intravesicular gradient of Na+ ions, a typical "overshoot" phenomenon in the accumulation pattern was observed. Osmotic manipulation of the incubation medium indicated that the transport of this bile acid occurs into an osmotically active intravesicular space. Uptake of taurocholate as measured after 1 min was specifically stimulated by Na+ ions: NaNO3 and NaCl were capable of supporting accumulation, whereas KNO3 was not. Na+-coupled uptake of taurocholate showed saturation kinetics and was inhibited by other bile acids or by preloading the vesicles with Na+. Our observations support the idea of a carrier-mediated bile-acid uptake system, as suggested previously for the intact rat liver and isolated rat hepatocytes. When the electrical potential difference across the vesicle membrane was changed by inducing different diffusion potentials (anion replacement), a more negative potential inside stimulated Na+-dependent taurocholate transport. The results demonstrate that rat-liver plasma membrane vesicles possess an electrogenic Na+-coupled transport system for taurocholate.
对从大鼠肝脏分离的质膜囊泡摄取牛磺胆酸盐的情况进行了研究。在存在胞外到胞内的钠离子梯度时，观察到积累模式中典型的“过冲”现象。对孵育介质进行渗透压操作表明，这种胆汁酸的转运发生在具有渗透活性的囊泡内空间。1分钟后测量的牛磺胆酸盐摄取受到钠离子的特异性刺激：硝酸钠和氯化钠能够支持积累，而硝酸钾则不能。钠离子偶联的牛磺胆酸盐摄取呈现饱和动力学，并受到其他胆汁酸或通过向囊泡预加载钠离子的抑制。我们的观察结果支持了载体介导的胆汁酸摄取系统的观点，正如之前对完整大鼠肝脏和分离的大鼠肝细胞所提出的那样。当通过诱导不同的扩散电位（阴离子置换）改变囊泡膜上的电势差时，囊泡内更负的电位会刺激钠离子依赖性牛磺胆酸盐的转运。结果表明，大鼠肝脏质膜囊泡具有一种一种电生钠离子偶联的牛磺胆酸盐转运系统。
