Mechanisms of taurocholate transport in canalicular and basolateral rat liver plasma membrane vesicles. Evidence for an electrogenic canalicular organic anion carrier.
Mechanisms of taurocholate transport in canalicular and basolateral rat liver plasma membrane vesicles. Evidence for an electrogenic canalicular organic anion carrier.
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DOI：
10.1016/s0021-9258(18)91006-9
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发表时间：
1984-08
期刊：
影响因子：
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通讯作者：
Peter J. Meiers;A. Meier-Abt;C. Barrett;J. Boyer
中科院分区：
文献类型：
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作者：
Peter J. Meiers;A. Meier-Abt;C. Barrett;J. Boyer
在高度纯化的小管（cLPM）和基底侧大鼠肝质膜（LPM）囊泡中测定牛磺胆酸盐转运的驱动力。还检查了丙氨酸转运以进行比较。间接的Na+而不是K+梯度瞬时刺激[3 H]牛磺胆酸盐（1 μ M）和[3 H]丙氨酸（0.2 mM）摄取到基底外侧LPM 3-4倍以上各自的平衡值（过冲）。Na+也刺激[3 H]牛磺胆酸盐的逆向转运和示踪剂交换在基底外侧LPM，而缬氨霉素诱导的内部负K+扩散电位刺激丙氨酸摄取，但对牛磺胆酸盐摄取没有影响。相反，在“右侧出”定向cLPM囊泡，[3 H]牛磺胆酸逆转运和示踪剂交换不依赖于Na+。[3 H]牛磺胆酸盐从cLPM的流出也不依赖于Na+，并且可以被囊外牛磺胆酸盐反式刺激。此外，一个内部负缬氨霉素介导的K+扩散电位抑制牛磺胆酸盐摄取到cLPM囊泡和刺激牛磺胆酸盐流出。这些研究为牛磺胆酸盐的小管排泄提供了“载体介导”和电位敏感的传导途径的直接证据。此外，他们证实了在肝细胞基底外侧膜中可能存在电中性Na+-牛磺胆酸盐共转运系统。
The driving forces for taurocholate transport were determined in highly purified canalicular (cLPM) and basolateral rat liver plasma membrane (LPM) vesicles. Alanine transport was also examined for comparison. Inwardly directed Na+ but not K+ gradients transiently stimulated [3H]taurocholate (1 microM) and [3H]alanine (0.2 mM) uptake into basolateral LPM 3-4- fold above their respective equilibrium values (overshoots). Na+ also stimulated [3H]taurocholate countertransport and tracer exchange in basolateral LPM whereas valinomycin-induced inside negative K+ diffusion potentials stimulated alanine uptake but had no effect on taurocholate uptake. In contrast, in the “right-side out” oriented cLPM vesicles, [3H]taurocholate countertransport and tracer exchange were not dependent on Na+. Efflux of [3H]taurocholate from cLPM was also independent of Na+ and could be trans-stimulated by extra-vesicular taurocholate. Furthermore, an inside negative valinomycin-mediated K+ diffusion potential inhibited taurocholate uptake into and stimulated taurocholate efflux from the cLPM vesicles. These studies provide direct evidence for a “carrier mediated” and potential-sensitive conductive pathway for the canalicular excretion of taurocholate. In addition, they confirm the presence of a possibly electroneutral Na+-taurocholate cotransport system in basolateral membranes of the hepatocyte.