Greger R, Schlatter E
Klin Wochenschr. 1983 Oct 17;61(20):1019-27. doi: 10.1007/BF01537500.
During the passed few years the cellular mechanisms responsible for the NaCl reabsorption in the thick ascending limb of the Henle loop of mammalian nephron and of the early distal tubule of amphibian kidney have been extensively studied. From these studies a new type of secondarily active transport mechanism, i.e. the Na+--2Cl- --K+ symport has emerged. Meanwhile it has been recognized that this system is also present in many other epithelia. All these epithelia share in common that they are sensitive to the so called loop diuretics. The present article summarizes our current knowledge of how the loop diuretics, by reversible interaction with the above cotransport system, inhibit the NaCl reabsorption in the thick ascending limb of Henle's loop. It is shown that these drugs transfer the thick ascending limb cell to a state in which not only transepithelial NaCl reabsorption ceases but in which also very little energy is consumed since then K+ and Cl- "relax" to passive distribution across both cell membranes and Na+ entry into the cell is blocked.
在过去几年中，人们对哺乳动物肾单位髓袢升支粗段和两栖类动物肾近端小管早期负责氯化钠重吸收的细胞机制进行了广泛研究。通过这些研究，一种新型的继发性主动转运机制，即Na⁺-2Cl⁻-K⁺协同转运体得以发现。同时，人们认识到该系统也存在于许多其他上皮组织中。所有这些上皮组织的共同特点是它们对所谓的袢利尿剂敏感。本文总结了我们目前对袢利尿剂如何通过与上述共转运系统的可逆相互作用来抑制髓袢升支粗段氯化钠重吸收的认识。结果表明，这些药物使髓袢升支粗段细胞进入一种状态，不仅跨上皮的氯化钠重吸收停止，而且此后消耗的能量也很少，因为钾离子和氯离子“松弛”到跨细胞膜的被动分布状态，同时钠离子进入细胞也被阻断。
