Acute effects of lead on the renal handling of zinc in dogs

Abstract

Urinary zinc excretion was monitored in anesthetized dogs before and during 4 hr after acute exposure to lead (doses: 0.3 mg Pb (as acetate)/kg as iv prime, followed by infusion of 0.057 mg Pb/min; 3mg Pb/kg, followed by 0.57 mg Pb/min as infusion; or equimolar sodium acetate in the control group). Zinc excretion in time controls was relatively constant over the 4 hr, but it rose above baseline values an average of 140 ng/min in 0.3 mg Pb/kg injected animals, and an average of 300 ng/min in 3 mg Pb/kg injected animals. Other indices of renal function, including excretion of protein, Na, K, and Mg, were relatively constant. Plasma Zn concentration was stable in time control and low Pb-administered animals, but rose significantly after the higher Pb dose. Clearance experiments using 65Zn and in vitro ultrafiltration of plasma were performed in another series of dogs under antidiuretic conditions. Zn excretion (monitored by 65Zn) was sevenfold higher in Pb-treated dogs; plasma Zn concentration was slightly, but not significantly, elevated. Ultrafiltrable Zn concentration was 2.5-fold higher and fractional Zn excretion was three times higher in Pb-treated dogs. The stop-flow pattern for Zn after Pb treatment showed no change in the distal tubular handling of Zn, but revealed prominent net proximal tubular secretion of Zn in all animals, a frequency statistically different from that observed in control animals. Thus, acute Pb treatment in dogs produced an increase in urinary Zn excretion which was related both to an increase in ultrafilterable plasma Zn and a change in renal tubular Zn transport. The plasma concentrations of insulin and glucagon were not altered by lead.