Activation of Na-H exchange by intracellular lithium in barnacle muscle fibers.
Activation of Na-H exchange by intracellular lithium in barnacle muscle fibers.
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藤壶肌纤维中细胞内锂激活 Na-H 交换。
DOI：
10.1152/ajpcell.1992.263.1.c246
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Boron,WF
中科院分区：
文献类型：
--
作者：
Davis,BA;Hogan,EM;Boron,WF
我们内部透析单藤壶肌纤维（BMF）90分钟的透析液（DF）不含Na+和0或100 mM的Li+和测量细胞内的pH值（pHi）与微电极。在透析过程中，pH 8.0的人工海水（ASW）不含Na+和HCO 3-。在我们停止用不含Li（+）/低pH DF透析并使pHi稳定在约6.8后，向ASW中加入440 mM Na（+）-10 mM HCO 3-使pHi迅速恢复并稳定在7.32。相反，当DF含有100 mM Li+时，pHi稳定在7.49。在透析到约7.2的pHi的纤维中，Li+刺激依赖于Na+但不受SITS影响的酸挤出的组分。因此，Li+激活了Na（+）依赖的酸挤出机制，而不是充分表征的Na（+）依赖的Cl-HCO 3交换剂。为了研究Li（+）激活机制，我们通过将pHDF提高到7.35并用SITS预处理BMF来最小化Na（+）依赖性Cl-HCO 3交换。我们发现，透析与Li+ eleva Na（+）依赖性pHi增加，这在很大程度上被阿米洛利阻断，与假设Li+激活潜在的Na-H交换，即使在正常的pHi。在不存在Li+的情况下，Na-H交换剂在pHi 7.35（净酸挤出速率，Jnet = 9.5 μ M/min）下相对无活性，但通过将pHi降低至6.8（Jnet = 64 μ M/min）而适度刺激。在Li+存在下，Na-H交换剂在7.35（Jnet = 141 μ M/min）和6.8（Jnet = 168 μ M/min）的pHi值下都非常活跃。因此Li+改变Na-H交换剂的pHi敏感性。由于Na-H交换剂的活性仅为Na（+）依赖性Cl-HCO 3交换剂活性的约6%，在不存在Li+且pH约为6.8的情况下，我们认为Na-H交换剂的主要作用可能不在于pH调节，而在于另一种功能，例如细胞体积调节。
We internally dialyzed single barnacle muscle fibers (BMF) for 90 min with a dialysis fluid (DF) containing no Na+ and either 0 or 100 mM Li+ and measured intracellular pH (pHi) with a microelectrode. During dialysis, the pH 8.0 artificial seawater (ASW) contained neither Na+ nor HCO3-. After we halted dialysis with a Li(+)-free/low-pH DF and allowed pHi to stabilize at approximately 6.8, adding 440 mM Na(+)-10 mM HCO3- to the ASW caused pHi to recover rapidly and stabilize at 7.32. In contrast, when the DF contained 100 mM Li+, pHi stabilized at 7.49. In fibers dialyzed to a pHi of approximately 7.2, Li+ stimulated a component of acid extrusion that was dependent on Na+ but not affected by SITS. Thus Li+ activates a Na(+)-dependent acid-extrusion mechanism other than the well characterized Na(+)-dependent Cl-HCO3 exchanger. To study the Li(+)-activated mechanism, we minimized Na(+)-dependent Cl-HCO3 exchange by raising pHDF to 7.35 and pretreated BMFs with SITS. We found that dialysis with Li+ elicits a Na(+)-dependent pHi increase that is largely blocked by amiloride, consistent with the hypothesis that Li+ activates a latent Na-H exchanger even at a normal pHi. In the absence of Li+, the Na-H exchanger is relatively inactive at pHi 7.35 (net acid-extrusion rate, Jnet = 9.5 microM/min) but modestly stimulated by reducing pHi to 6.8 (Jnet = 64 microM/min). In the presence of Li+, the Na-H exchanger is very active at pHi values of both 7.35 (Jnet = 141 microM/min) and 6.8 (Jnet = 168 microM/min). Thus Li+ alters the pHi sensitivity of the Na-H exchanger. Because the Na-H exchanger is only approximately 6% as active as the Na(+)-dependent Cl-HCO3 exchanger in the absence of Li+ at a pHi of approximately 6.8, we suggest that the major role of the Na-H exchanger may not be in pHi regulation but in another function such as cell-volume regulation.
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