Atherton J C, Green R, Higgins A, Large A, McNicholas C, Parker D, Pempkowiak L, Rajani K, Smith J
Department of Physiological Sciences, Manchester University, England, United Kingdom.
Kidney Int Suppl. 1990 Mar;28:S36-8.
In summary, our experiments clearly demonstrate that lithium reabsorption occurs by frusemide- and bumetanide-sensitive reabsorption, but we have failed to identify the mechanism(s) responsible for the lower CLi and FELi in salt-depletion. It is possible that some, as yet unknown, factor increases the activity of the Na, K, 2Cl cotransporter and, hence, increases lithium reabsorption in the thick ascending limb in salt-depleted subjects. However, it is equally possible that a fraction of proximal tubular reabsorption is inhibited by frusemide and bumetanide. If this is correct, CLi in humans are reasonable markers of proximal tubular function even in conditions of avid salt retention and in salt depletion, when fractional reabsorption of salt and water in the proximal tubules is enhanced.
总之,我们的实验清楚地表明,锂的重吸收是通过对速尿和布美他尼敏感的重吸收过程发生的,但我们未能确定导致盐耗竭时锂清除率(CLi)降低和锂排泄分数(FELi)降低的机制。有可能存在某种尚未知晓的因素会增加钠 - 钾 - 2氯协同转运体的活性,从而增加盐耗竭受试者厚壁升支中锂的重吸收。然而,同样有可能的是,速尿和布美他尼会抑制近端小管重吸收的一部分。如果这是正确的,那么即使在盐潴留活跃和盐耗竭的情况下,当近端小管中盐和水的重吸收分数增加时,人体中的CLi仍是近端小管功能的合理标志物。