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氰化物对蛙近端肾小管周细胞跨膜表观钾电导的影响。

The effect of cyanide on apparent potassium conductance across the peritubular cell membrane of frog proximal tubules.

作者信息

Rehwald W, Lang F

出版信息

Pflugers Arch. 1986 Dec;407(6):607-10. doi: 10.1007/BF00582639.

Abstract

To test for the effect of cyanide on frog proximal renal tubules the potential difference across the peritubular cell membrane (PDpt) has been recorded continuously before and during peritubular application of 1 mmol/l cyanide using conventional microelectrodes. Before application of cyanide PDpt amounts to -61.5 +/- 2.2 mV in the absence of luminal substrate. Cyanide depolarizes the peritubular cell membrane by +18.8 +/- 2.3 mV/10 min in the presence and by +4.5 +/- 0.9 mV/10 min in the absence of luminal substrate. The rapid depolarization of the cell membranes to addition of glucose to luminal perfusate is not significantly influenced by exposure to cyanide, whereas the influence of altered peritubular potassium concentration (from 3 to 9 mmol/l) is significantly reduced from +15.2 +/- 1.7 mV to +8.7 +/- 1.8 mV. Following exposure to cyanide the lumped resistance of the luminal and peritubular cell membranes increases significantly by 36 +/- 7%/6 min, and the cellular core resistance significantly by 14 +/- 6%/6 min. As a result, cyanide markedly decreases the peritubular potassium conductance, depolarizes the cell membranes and reduces the driving force for sodium coupled transport processes. Thus cyanide fully mimics the effects of ouabain, although cyanide in contrast to ouabain is expected to deplete the cells from ATP. In conclusion ATP/ADP is not likely to play a major role in the regulation of sodium coupled transport processes and peritubular potassium conductance in amphibian proximal tubules.

摘要

为了测试氰化物对青蛙近端肾小管的影响,使用传统微电极在管周应用1 mmol/l氰化物之前和期间,连续记录跨管周细胞膜的电位差(PDpt)。在没有管腔底物的情况下,施加氰化物之前PDpt为-61.5±2.2 mV。在有管腔底物存在时,氰化物使管周细胞膜去极化,速率为+18.8±2.3 mV/10分钟;在没有管腔底物时,速率为+4.5±0.9 mV/10分钟。向管腔灌注液中添加葡萄糖时细胞膜的快速去极化不受氰化物暴露的显著影响,而管周钾浓度改变(从3 mmol/l到9 mmol/l)的影响则从+15.2±1.7 mV显著降低至+8.7±1.8 mV。暴露于氰化物后,管腔和管周细胞膜的总电阻在6分钟内显著增加36±7%,细胞核心电阻在6分钟内显著增加14±6%。结果,氰化物显著降低管周钾电导,使细胞膜去极化,并降低钠偶联转运过程的驱动力。因此,氰化物完全模拟了哇巴因的作用,尽管与哇巴因不同,预计氰化物会使细胞内ATP耗竭。总之,ATP/ADP在两栖动物近端小管钠偶联转运过程和管周钾电导的调节中不太可能起主要作用。

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