Wright F S
Fed Proc. 1981 Jul;40(9):2398-402.
Potassium excreted by the kidney is derived largely from potassium secretion by the distal tubule and collecting duct. It is this secreted fraction that responds to systemic changes and is mainly responsible for regulation of potassium balance. A smaller fraction of the excreted quantity comes from potassium that is filtered and escapes reabsorption. Variations in the rate of reabsorption may alter potassium secretion under some circumstances. In the proximal tubule, reabsorption of potassium appears to involve interaction with a membrane mechanism. The contribution of descending limb potassium secretion to final potassium secretion is a present uncertain because of the inaccessibility of inner cortical distal tubules and collecting ducts in intact animals. Changes in plasma K, plasma aldosterone, and plasma acidity all appear to affect distal potassium secretion by influencing the uptake of potassium from blood to cell and thus raising the intracellular potassium. Changes in extracellular fluid volume, which increase urine flow and sodium excretion, appear to increase distal potassium secretion as a consequence of increases in the flow rate of luminal fluid. Flow-dependent changes in luminal potassium concentration may be involved but they do not appear to act by simply increasing the passive electrochemical driving force (assessed across the entire epithelium). Our understanding of the cellular mechanisms controlling renal potassium secretion is becoming clearer as it becomes possible to identify and to separate for a study a potentially confusing array of interacting variables.
肾脏排泄的钾主要来源于远端小管和集合管的钾分泌。正是这一分泌部分对全身变化做出反应,并且主要负责钾平衡的调节。排泄量的一小部分来自滤过且未被重吸收的钾。在某些情况下,重吸收率的变化可能会改变钾分泌。在近端小管中,钾的重吸收似乎涉及与一种膜机制的相互作用。由于完整动物体内皮质内远端小管和集合管难以接近,目前尚不确定降支钾分泌对最终钾分泌的贡献。血浆钾、血浆醛固酮和血浆酸度的变化似乎都通过影响钾从血液到细胞的摄取从而提高细胞内钾,进而影响远端钾分泌。细胞外液量的变化会增加尿流量和钠排泄,似乎会因管腔液流速增加而增加远端钾分泌。管腔钾浓度的流量依赖性变化可能参与其中,但它们似乎并非仅仅通过增加被动电化学驱动力(跨整个上皮评估)起作用。随着能够识别并分离一系列可能令人困惑的相互作用变量以供研究,我们对控制肾脏钾分泌的细胞机制的理解正变得更加清晰。