Welling P A
Department of Physiology, University of Maryland School of Medicine, Baltimore, USA.
Kidney Int. 1995 Oct;48(4):1017-23. doi: 10.1038/ki.1995.384.
Over the last few years it has become evident that an assortment of functionally-related, but diverse, KATP channels provide an important and physiologically-regulated determinant of the K conductive pathways in many, if not all, epithelial cells expressed along the nephron. As such, KATP plays central roles in regulating and maintaining a number of transport processes in concert with physiological demands of the kidney. In the renal proximal tubule, KATP channels and changes in the hydrolytic activity of the Na,K-ATPase permit ATP to act as a coupling modulator of parallel Na,K-ATPase-K recycling. The response insures that cell membrane potential, intracellular K activity and cell volume are protected in the face of physiological variations in transcellular ion transport. In addition to demonstrating the physiological relevance of KATP in renal epithelial, these studies have provided a long awaited answer to the underlying mechanism of pump-leak coupling, a universal and essential homeostatic mechanism observed in nearly all salt translocating epithelia.
在过去几年中,显而易见的是,多种功能相关但各异的钾离子通道(KATP通道)在许多(即便不是所有)沿肾单位表达的上皮细胞中,为钾离子传导途径提供了一个重要且受生理调节的决定因素。因此,KATP通道在协同肾脏的生理需求来调节和维持多种转运过程中发挥着核心作用。在近端肾小管中,KATP通道以及钠钾ATP酶水解活性的变化使得ATP能够作为平行的钠钾ATP酶 - 钾离子循环的偶联调节剂。这种反应确保了在跨细胞离子转运发生生理变化时,细胞膜电位、细胞内钾离子活性以及细胞体积能够得到保护。除了证明KATP通道在肾上皮细胞中的生理相关性外,这些研究还为泵 - 漏偶联的潜在机制提供了期待已久的答案,泵 - 漏偶联是一种在几乎所有盐分转运上皮细胞中都能观察到的普遍且基本的稳态机制。