由Na+/K+ATPase活性建立的钠(Na+)电化学梯度驱动离子的转运,矿物,和糖在兴奋和非兴奋细胞。Na依赖性转运蛋白可以沿相同方向(共转运)或相反方向(交换剂)移动这些溶质,穿过极化上皮的顶端和基底外侧质膜。除了维持这些溶质的生理稳态外,钠的增加和减少也可能引发,直接或间接,调节各种细胞内翻译后事件的信号级联。在这次审查中,我们将描述Na+/K+ATPase如何维持钠依赖性转运机制利用的Na+梯度来调节葡萄糖摄取,兴奋性神经递质,钙信号,酸碱平衡,盐消耗障碍,流体体积,镁运输。我们将讨论几种Na依赖性共转运蛋白和Na依赖性交换剂如何在人类健康和疾病中发挥重要作用。最后,我们将讨论这些依赖Na+的转运机制是如何被证明或有可能将Na+用作信号分子的次要作用。
Sodium (Na+) electrochemical gradients established by Na+/K+ ATPase activity drives the transport of ions, minerals, and sugars in both excitable and non-excitable cells. Na+-dependent transporters can move these solutes in the same direction (cotransport) or in opposite directions (exchanger) across both the apical and basolateral plasma membranes of polarized epithelia. In addition to maintaining physiological homeostasis of these solutes, increases and decreases in sodium may also initiate, directly or indirectly, signaling cascades that regulate a variety of intracellular post-translational events. In this review, we will describe how the Na+/K+ ATPase maintains a Na+ gradient utilized by multiple sodium-dependent transport mechanisms to regulate glucose uptake, excitatory neurotransmitters, calcium signaling, acid-base balance, salt-wasting disorders, fluid volume, and magnesium transport. We will discuss how several Na+-dependent cotransporters and Na+-dependent exchangers have significant roles in human health and disease. Finally, we will discuss how each of these Na+-dependent transport mechanisms have either been shown or have the potential to use Na+ in a secondary role as a signaling molecule.