Effects of hyperosmotic medium on hepatocyte volume, transmembrane potential and intracellular K+ activity.
Effects of hyperosmotic medium on hepatocyte volume, transmembrane potential and intracellular K+ activity.
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高渗介质对肝细胞体积、跨膜电位和细胞内 K 活性的影响。
DOI：
10.1016/0005-2736(91)90123-p
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Wondergem,R
中科院分区：
文献类型：
--
作者：
Wang,KN;Wondergem,R
肝细胞跨膜电位(Vm)是一种渗透压计，随着细胞外渗透压的变化而变化(Howard，L.D.和Wondergem，R.(1987)J.Membr)。比奥尔。100，53)。我们现在已经证明了通过添加蔗糖增加体外渗透压和不改变离子强度来对Vm产生类似的影响。我们还证明，高渗应激诱导的Vm的去极化是由于膜K+电导Gk的变化，而不是K+平衡电位的变化。分别用常规和离子敏感微电极测量肝切片中肝细胞的Vmandaki。细胞水伏。通过孵育10分钟后肝脏切片的湿重和干重的差异来估计。通过对外界[K+]阶跃变化Vmf的影响来衡量高渗介质对膜K+转移数tk的影响。高渗加蔗糖(50、100和150 mM)的高渗液灌流后，肝细胞Vm分别下降34、52和54%。相应地，添加蔗糖的高渗胁迫下，aKI分别增加了10%、18%和29%。添加50、100和150 mM蔗糖后，对照组组织水由2.92±0.10 kg/kg干重分别降至2.60±0.05、2.25±0.06和2.22±0.05 kg/kg干重。加入50 mM蔗糖后，tK由0.20±0.01降至0.05±0.01。在无氯介质中，用葡萄糖酸取代Cl-−，在高渗胁迫(100 mM蔗糖)下也可发生50%的去极化。我们的结论是，在高渗应激时，肝细胞收缩，而肝细胞增殖。随之而来的Vm的下降与Inaki的增加所预期的相反，至少部分原因是伴随着K的下降。膜氯−电导的改变很可能不是渗透胁迫诱导的去极化的原因，因为在用无氯介质灌流组织来耗尽氯−的细胞中，添加蔗糖使V值降低。
Hepatocyte transmembrane potential (Vm) behaves as an osmometer and varies with changes in extracellular osmotic pressure created by altering the NaCl concentration in the external medium (Howard, L.D. and Wondergem, R. (1987) J. Membr. Biol. 100, 53). We now have demonstrated similar effects onVmby increasing external osmolality with added sucrose and not altering ionic strength. We also have demonstrated that hyperosmotic stress-induced depolarization ofVmresults from changes in membrane K+conductance,gK, rather than from changes in the K+equilibrium potential.Vmandakiof hepatocytes in liver slices were measured by conventional and ion-sensitive microelectrodes, respectively. Cell water vols. were estimated by differences in wet and dry weights of liver slices after 10-min incubations. Effect of hyperosmotic medium on membrane transference number for K+,tk, was measured by effects onVmof step-changes in external [K+]. HepatocyteVmdecreased 34, 52 and 54% when tissue was superfused with medium made hyperosmotic with added sucrose (50, 100 and 150 mM). Correspondingly,aKiincreased 10, 18 and 29% with this hyperosmotic stress of added sucrose. Tissue water of2.92 ± 0.10 kg H2O/kg dry weight in control solution decreased to 2.60 ± 0.05, 2.25 ± 0.06and2.22 ± 0.05 kg H2O/kg dry weight with additions to medium of 50, 100 and 150 mM sucrose, respectively. Adding 50 mM sucrose to medium decreasedtKfrom 0.20 ± 0.01 to 0.05 ± 0.01. Depolarization by 50% with hyperosmotic stress (100 mM sucrose) also occurred in Cl-free medium where Cl−was substituted with gluconate. We conclude that hepatocytes shrink during hyperosmotic stress, and theaKiincreases. The accompanying decrease inVmis opposite to that expected by an increase inaKi, and at least in part results from a concomitant decrease ingK. Changes in membrane Cl−conductance most likely do not contribute to osmotic stress-induced depolarization, since equivalent decreases inVmoccurred with added sucrose in cells depleted of Cl−by superfusing tissue with Cl-free medium.
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细胞钙和跨膜电位参与肝细胞体积的控制
影响因子：
13.5
作者：
W. Khalbuss;R. Wondergem
通讯作者：
R. Wondergem
用微电极测量小鼠肝脏切片中细胞内氯离子的活性。
DOI：
10.1016/0005-2736(87)90155-6
发表时间：
1987
期刊：
Biochimica et biophysica acta
影响因子：
--
作者：
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通讯作者：
Armstrong,WM
离体大鼠肝细胞的钾渗透性和体积控制。
DOI：
10.1016/0005-2736(83)90014-7
发表时间：
1983
期刊：
Biochimica et biophysica acta
影响因子：
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作者：
T. Bakker
通讯作者：
T. Bakker
DOI：
10.1016/0005-2736(90)90435-q
发表时间：
1990
期刊：
Biochimica et biophysica acta
影响因子：
--
作者：
W. Khalbuss;R. Wondergem
通讯作者：
R. Wondergem