|
pubmed:abstractText |
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.
|
