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首页> 美国卫生研究院文献>American Journal of Physiology - Renal Physiology >Ouabain stimulates Na-K-ATPase through a sodium/hydrogen exchanger-1 (NHE-1)-dependent mechanism in human kidney proximal tubule cells
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Ouabain stimulates Na-K-ATPase through a sodium/hydrogen exchanger-1 (NHE-1)-dependent mechanism in human kidney proximal tubule cells

机译：哇巴因通过人肾近端肾小管细胞中的钠/氢交换子1（NHE-1）依赖性机制刺激Na​​-K-ATPase

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Recent investigations demonstrate increased Na/H exchanger-1 (NHE-1) activity and plasma levels of ouabain-like factor in spontaneously hypertensive rats. At nanomolar concentrations, ouabain increases Na-K-ATPase activity, induces cell proliferation, and activates complex signaling cascades. We hypothesize that the activity of NHE-1 and Na-K-ATPase are interdependent. To test whether treatment with picomolar ouabain regulates Na-K-ATPase through an NHE-1-dependent mechanism, we examined the role of NHE-1 in ouabain-mediated stimulation of Na-K-ATPase in kidney proximal tubule cell lines [opossum kidney (OK), HK-2, HKC-5, and HKC-11] and rat kidney basolateral membranes. Ouabain stimulated Na-K-ATPase activity and tyrosine phosphorylation in cells that express NHE-1 (OK, HKC-5, and HKC-11) but not in HK-2 cells that express very low levels of NHE-1. Inhibition of NHE-1 with 5 μM EIPA, a NHE-1-specific inhibitor, prevented ouabain-mediated stimulation of 86Rb uptake and Na-K-ATPase phosphorylation in OK, HKC-5, and HKC-11 cells. Expression of wild-type NHE-1 in HK2 cells restored regulation of Na-K-ATPase by picomolar ouabain. Treatment with picomolar ouabain increased membrane expression of Na-K-ATPase and enhanced NHE-1-Na-K-ATPase α1-subunit association. Treatment with ouabain (1 μg·kg body wt−1·day−1) increased Na-K-ATPase activity, expression, phosphorylation, and association with NHE-1 increased in rat kidney cortical basolateral membranes. Eight days' treatment with ouabain (1 μg·kg body wt−1·day−1) resulted in increased blood pressure in these rats. These results suggest that the association of NHE-1 with Na-K-ATPase is critical for ouabain-mediated regulation of Na-K-ATPase and that these effects may play a role in cardioglycoside-stimulated hypertension.
机译：最近的研究表明，自发性高血压大鼠的Na / H交换器1（NHE-1）活性和哇巴因样因子的血浆水平升高。在纳摩尔浓度下，哇巴因增加Na-K-ATPase活性，诱导细胞增殖，并激活复杂的信号级联反应。我们假设NHE-1和Na-K-ATPase的活性是相互依赖的。为了测试皮摩尔哇巴因的处理是否通过NHE-1依赖性机制调节Na-K-ATPase，我们检查了NHE-1在哇巴因介导的肾近端肾小管细胞系[负鼠肾]刺激中的作用。 （OK），HK-2，HKC-5和HKC-11]和大鼠肾脏基底外侧膜。哇巴因在表达NHE-1（OK，HKC-5和HKC-11）的细胞中刺激Na-K-ATPase活性和酪氨酸磷酸化，但在表达NHE-1水平非常低的HK-2细胞中却没有。用5μMEIPA（一种NHE-1特异性抑制剂）抑制NHE-1，可以阻止哇巴因介导的OK，HKC-5和HKC刺激 86 Rb摄取和Na-K-ATPase磷酸化-11个细胞。 HK2细胞中野生型NHE-1的表达恢复了皮摩尔哇巴因对Na-K-ATPase的调节。皮摩尔哇巴因处理可增加Na-K-ATPase的膜表达，并增强NHE-1-Na-K-ATPaseα1-亚基的缔合。哇巴因（1μg·kg体重 −1 ·天 -1 ）治疗增加了Na-K-ATPase的活性，表达，磷酸化以及与NHE-1的结合在大鼠肾脏皮质基底外侧膜中。用哇巴因治疗八天（1μg·kg体重 -1 ·天 -1 ）导致这些大鼠血压升高。这些结果表明，NHE-1与Na-K-ATPase的结合对于哇巴因介导的Na-K-ATPase的调控至关重要，并且这些作用可能在糖苷刺激的高血压中起作用。

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