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首页> 外文期刊>Biochimica et biophysica acta. Molecular basis of disease: BBA >The sodium pump and cardiotonic steroids-induced signal transduction protein kinases and calcium-signaling microdomain in regulation of transporter trafficking.
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The sodium pump and cardiotonic steroids-induced signal transduction protein kinases and calcium-signaling microdomain in regulation of transporter trafficking.

机译：钠泵和强心类固醇诱导的信号转导蛋白激酶和钙信号转导微区调节转运蛋白的运输。

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摘要

The Na/K-ATPase was discovered as an energy transducing ion pump. A major difference between the Na/K-ATPase and other P-type ATPases is its ability to bind a group of chemicals called cardiotonic steroids (CTS). The plant-derived CTS such as digoxin are valuable drugs for the management of cardiac diseases, whereas ouabain and marinobufagenin (MBG) have been identified as a new class of endogenous hormones. Recent studies have demonstrated that the endogenous CTS are important regulators of renal Na(+) excretion and blood pressure. The Na/K-ATPase is not only an ion pump, but also an important receptor that can transduce the ligand-like effect of CTS on intracellular protein kinases and Ca(2+) signaling. Significantly, these CTS-provoked signaling events are capable of reducing the surface expression of apical NHE3 (Na/H exchanger isoform 3) and basolateral Na/K-ATPase in renal proximal tubular cells. These findings suggest that endogenous CTS may play an important role in regulation of tubular Na(+) excretion under physiological conditions; conversely, a defect at either the receptor level (Na/K-ATPase) or receptor-effector coupling would reduce the ability of renal proximal tubular cells to excrete Na(+), thus culminating/resulting in salt-sensitive hypertension.
机译：Na / K-ATPase被发现是一种能量转导离子泵。 Na / K-ATPase与其他P型ATPase之间的主要区别在于其结合一组称为强心类固醇（CTS）的化学物质的能力。植物来源的CTS（例如地高辛）是治疗心脏病的有价值的药物，而哇巴因和marinobufagenin（MBG）已被鉴定为一类新的内源激素。最近的研究表明，内源性CTS是肾脏Na（+）排泄和血压的重要调节剂。 Na / K-ATPase不仅是离子泵，而且是重要的受体，可以转导CTS对细胞内蛋白激酶和Ca（2+）信号的配体样作用。值得注意的是，这些由CTS引起的信号转导事件能够减少肾脏近端肾小管细胞中根尖NHE3（Na / H交换异构体3）和基底外侧Na / K-ATPase的表面表达。这些发现表明内源性CTS可能在生理条件下在调节肾小管Na（+）排泄中起重要作用。相反，受体水平（Na / K-ATPase）或受体效应子偶联的缺陷会降低肾近端小管细胞排泄Na（+）的能力，从而最终导致/导致盐敏感性高血压。

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