Bertorello A M, Katz A I
Rolf Luft Center for Diabetes Research, Department of Endocrinology, Karolinska Institutet, Karolinska Hospital, Stockholm, Sweden.
Am J Physiol. 1993 Dec;265(6 Pt 2):F743-55. doi: 10.1152/ajprenal.1993.265.6.F743.
Sodium-potassium-activated adenosinetriphosphatase (Na-K-ATPase; the Na:K pump), located at the basolateral domain of epithelial cells, provides the driving force for active sodium and potassium translocation and for the secondary active transport of other solutes across the renal tubules. Short-term regulation of renal Na-K-ATPase activity (i.e., not reflecting changes in its biosynthesis rate) provides an important mechanism of modulating tubule transport and thus the final Na and K urinary excretion. Recent studies have provided abundant evidence that such regulation is effected by complex functional networks that are specific for different nephron segments and involve distinct and often mutually interacting intracellular signal transduction pathways. The effects of hormones and autacoids linked to alterations in cell adenosine 3',5'-cyclic monophosphate and consequently of protein kinase A, in the levels and distribution of protein kinase C, or in the generation of various eicosanoids provide examples of rapid Na:K pump activity modulation by the mechanisms mentioned above. In this review we assess the roles of specific intracellular messengers and the manner in which they, and especially protein kinases, might interact with the pump in the short-term regulation of its activity; also, we examine the emerging evidence supporting the participation of the cytoskeleton in this process.
钠钾激活的三磷酸腺苷酶（Na-K-ATP酶；钠钾泵）位于上皮细胞的基底外侧区域，为钠和钾的主动转运以及其他溶质跨肾小管的继发性主动转运提供驱动力。肾Na-K-ATP酶活性的短期调节（即不反映其生物合成速率的变化）是调节肾小管转运从而最终调节尿钠和钾排泄的重要机制。最近的研究提供了大量证据表明，这种调节是由复杂的功能网络实现的，这些网络对不同的肾单位节段具有特异性，并且涉及不同的且常常相互作用的细胞内信号转导途径。与细胞3',5'-环磷酸腺苷改变相关的激素和自分泌物质，进而与蛋白激酶A、蛋白激酶C的水平和分布改变，或各种类花生酸生成改变相关的激素和自分泌物质，提供了通过上述机制快速调节钠钾泵活性的实例。在本综述中，我们评估了特定细胞内信使的作用以及它们，尤其是蛋白激酶，在其活性的短期调节中可能与泵相互作用的方式；此外，我们研究了支持细胞骨架参与这一过程的新证据。
