Hepatic taurocholate uptake is electrogenic and influenced by transmembrane potential difference.
Hepatic taurocholate uptake is electrogenic and influenced by transmembrane potential difference.
复制标题
肝脏牛磺胆酸盐的摄取是生电的并受跨膜电位差的影响。
DOI：
10.1152/ajpgi.1993.264.3.g478
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Scharschmidt,BF
中科院分区：
文献类型：
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作者：
Lidofsky,SD;Fitz,JG;Weisiger,RA;Scharschmidt,BF
肝细胞对胆汁酸牛磺胆酸盐的摄取与Na+流入相关。然而，摄取的化学计量是不确定的，跨膜电位差（PD）对此过程的影响也是不确定的。在本研究中，我们研究了灌注肝脏中牛磺胆酸盐提取与PD（使用细胞内微电极测量）之间的关系，并使用膜片钳记录技术测量了培养肝细胞中牛磺胆酸盐诱导的传输电流。在基础条件下的灌注肝脏中，PD 平均为 -28.4 +/- 0.6 (SE) mV，1、50 和 300 microM 牛磺胆酸盐的提取分别为 0.95 +/- 0.02、0.98 +/- 0.01 和 0.41 +/- 0.03。当用胆碱替代灌注液 Na+ 来降低 Na+ 化学梯度时，膜去极化至 -17.2 +/- 1.1 mV，并且在所有牛磺胆酸盐浓度下，牛磺胆酸盐提取量均显着降低 (P < 0.01)。当灌流液 Na+ 浓度保持恒定在 137 mM 时，用葡萄糖酸盐替代灌流液 Cl- (-17.9 +/- 0.6 mV) 或用 Cl- 替代硝酸盐 (-10.3 +/- 2.1 mV) 引起的膜去极化显着降低了 300 microM 牛磺胆酸盐的提取。在 Na+ 存在的情况下，突然接触牛磺胆酸盐会产生浓度依赖性膜去极化，但在 Na+ 不存在的情况下则不会产生浓度依赖性膜去极化（P < 0.001）。在培养的肝细胞中，暴露于 100 µM 牛磺胆酸盐，在 -40 mV 的保持电位下产生 -0.056 +/- 0.016 pA/pF 的内向电流。该电流依赖于 Na+，并且当保持电位从 -20 变为 -50 mV 时，电流增加两倍。（摘要截断为 250 字）
Uptake of the bile acid taurocholate by hepatocytes is coupled to Na+ influx. The stoichiometry of uptake, however, is uncertain, as is the influence of the transmembrane electrical potential difference (PD) on this process. In this study, we examined the relationship between taurocholate extraction and PD (measured using intracellular microelectrodes) in perfused liver, and we measured taurocholate-induced transport current in cultured hepatocytes using patch-clamp recording techniques. In the perfused liver under basal conditions, PD averaged -28.4 +/- 0.6 (SE) mV, and extraction of 1, 50, and 300 microM taurocholate was 0.95 +/- 0.02, 0.98 +/- 0.01, and 0.41 +/- 0.03, respectively. When the Na+ chemical gradient was decreased by replacing perfusate Na+ with choline, the membrane depolarized to -17.2 +/- 1.1 mV, and taurocholate extraction markedly decreased at all taurocholate concentrations (P < 0.01). When perfusate Na+ concentration was held constant at 137 mM, membrane depolarization induced by substitution of gluconate for perfusate Cl- (-17.9 +/- 0.6 mV) or Cl- for nitrate (-10.3 +/- 2.1 mV) significantly decreased extraction of 300 microM taurocholate. Abrupt exposure to taurocholate produced a concentration-dependent membrane depolarization in the presence of Na+, but not in its absence (P < 0.001). In cultured hepatocytes, exposure to 100 microM taurocholate produced an inward current of -0.056 +/- 0.016 pA/pF at a holding potential of -40 mV. This current was Na+ dependent, and it increased twofold as holding potential was changed from -20 to -50 mV.(ABSTRACT TRUNCATED AT 250 WORDS)