Silva P, Hayslett J P, Epstein F H
J Clin Invest. 1973 Nov;52(11):2665-71. doi: 10.1172/JCI107460.
The specific activity of sodium-potassium-activated adenosine triphosphatase (Na-K-ATPase) in homogenates of rat kidneys increases when the dietary intake of potassium is chronically increased. The effect is seen first and is most prominent in the outer medulla, but large loads of potassium elicit an increase in the cortex as well. Levels of Na-K-ATPase in brian, liver, and muscle, by contrast, are unaffected by potassium loading. Although the changes in enzyme activity in the kidney resemble those reportedly produced by aldosterone, they are not induced by experimental sodium deprivation, and they can be evoked by potassium loading in the absence of the adrenal glands. The results suggest that Na-K-ATPase of renal tubular cells, presumably in the distal tubules and collecting ducts, plays an important role in the phenomenon of potassium adaptation and in the process by which potassium is excreted into the urine.
当长期增加钾的饮食摄入量时,大鼠肾脏匀浆中钠钾激活的三磷酸腺苷酶(Na-K-ATP酶)的比活性会增加。这种效应首先出现在外髓质,且最为显著,但大量的钾也会引起皮质中该酶活性增加。相比之下,大脑、肝脏和肌肉中的Na-K-ATP酶水平不受钾负荷的影响。尽管肾脏中酶活性的变化类似于据报道由醛固酮产生的变化,但它们不是由实验性钠缺乏诱导的,并且在没有肾上腺的情况下,钾负荷也能引发这种变化。结果表明,肾小管细胞(可能是远端小管和集合管中的细胞)的Na-K-ATP酶在钾适应现象以及钾排泄到尿液的过程中起重要作用。