Effect of cadmium on renal tubular sodium transport

Abstract

The discovery of a cadmium-containing protein, metallothionein, in renal cortex prompted these experiments, performed on anesthetized dogs undergoing saline diuresis. Both ureters were catheterized, and standard clearance techniques were employed. After completion of at least three control clearance periods, cadmium (as CdCl₂), 0.35–4.46 µm/kg, was infused i.v. over 10 min. Cysteine was also infused to prevent or minimize blood pressure, glomerular filtration rate (GFR), and renal plasma flow decreases induced by cadmium. After all 17 injections, sodium excretion decreased, (U_NaV)_cont – (U_NaV)_Cd = 46–275 µm/min. The dose-response curve appeared to be hyperbolic; peak effect was usually 30 min after injection; range was 15–50 min. There was no change in GFR during these same periods; the average GFR ratio (Cd/control) for all experiments was 1.01 ± 0.03. Plasma sodium also was unchanged. Direct left renal artery infusion of cadmium produced increased sodium reabsorption, either limited to the left or greater than that on the right. These experiments establish the ability of cadmium to increase tubular sodium reabsorption by a direct renal effect.