Zinc and the sodium pump in uremia.
A defect in sodium transport is known to exist in the leucocytes of uremic patients. Recent work has shown changes in cation flux rates associated with alterations of extracellular zinc concentration. As plasma zinc is known to be low in uremia, the possibility that this might be the cause of the defect in membrane transport was investigated. Plasma zinc was shown to be lower in uremic patients than in normal controls but this was not matched by alterations in leucocyte zinc content. Leucocytes from normal subjects and from patients with uremia have similar increases in the sodium efflux rate constant when exposed to elevated extracellular zinc concentrations. However, the abnormality in leucocyte sodium transport in uremia was not completely corrected by elevation of the extracellular zinc, when compared with normal cells in the same zinc concentrations. Although extracellular zinc is a factor that must be controlled in studies of cellular membrane transport, a low plasma zinc is not the explanation for the defect of sodium transport seen in uremia.
D001692:Biological Transport / Q000187:drug effects; D006801:Humans; D010042:Ouabain / Q000494:pharmacology; D012964:Sodium / Q000378:metabolism*; D014511:Uremia / Q000097:blood / Q000378:metabolism*; D015032:Zinc / Q000097:blood*
D010042:Ouabain; D012964:Sodium; D015032:Zinc