Taurocholate transport by rat liver canalicular membrane vesicles. Evidence for the presence of an Na+-independent transport system.
Taurocholate transport by rat liver canalicular membrane vesicles. Evidence for the presence of an Na+-independent transport system.
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DOI：
10.1172/jci111257
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发表时间：
1984-03
期刊：
影响因子：
--
通讯作者：
Masayasu Inoue
中科院分区：
文献类型：
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作者：
Masayasu Inoue
为了阐明胆汁酸在肝脏中的载体转运机制，用快速滤膜法研究了牛磺胆酸盐在肝小管膜泡中的转运。膜小泡显示牛磺胆酸盐向渗透反应性囊腔内的转运依赖于温度，不依赖于Na+。在无钠条件下，牛磺胆酸的摄取遵循饱和动力学(37℃时，表观Km=43微米，Vmax=0.22nmol/mg蛋白X 20 S)，并被胆酸盐和丙磺舒抑制。未标记牛磺胆酸盐的反式刺激也被证实。当通过阴离子置换改变跨膜的电势差时，小泡对牛磺胆酸盐的运输有较正的刺激电位和较负的抑制电位。瓦林霉素诱导的K+扩散电位(囊泡内阳性)增加了牛磺胆酸的摄取速率，但不受施加的pH梯度的影响。这些结果表明，大鼠肝小管质膜含有一个不依赖于钠的牛磺胆酸盐转运系统，它能将胆汁酸作为阴离子跨膜转运。在完整的肝细胞中，跨小管膜的电位差可能为牛磺胆酸的分泌提供了驱动力。非离子扩散对牛磺胆酸分泌的贡献似乎很小。
To elucidate the mechanism of vectorial translocation of bile acids in the liver, taurocholate transport was studied in isolated liver canalicular membrane vesicles by a rapid filtration method. The membrane vesicles revealed temperature-dependent, Na+-independent transport of taurocholate into an osmotically reactive intravesicular space. In the absence of sodium, taurocholate uptake followed saturation kinetics (apparent Km for taurocholate = 43 microM and Vmax = 0.22 nmol/mg protein X 20 s at 37 degrees C) and was inhibited by cholate and probenecid. Transstimulation by unlabeled taurocholate was also demonstrated. When the electrical potential difference across the membranes was altered by anion replacement, a more positive intravesicular potential stimulated, and a more negative potential inhibited, transport of taurocholate by the vesicles. Valinomycin-induced K+-diffusion potential (vesicle inside-positive) enhanced the rate of taurocholate uptake that was not altered by imposed pH gradients. These results indicate that rat liver canalicular plasma membrane contains a sodium-independent taurocholate transport system that translocates the bile acid as an anion across the membrane. In intact hepatocytes, the electrical potential difference across the canalicular membrane probably provides the driving force for taurocholate secretion. The contribution of nonionic diffusion to taurocholate secretion appears to be minimal.