Vanadium‐induced inhibition of renal na+, k+‐adenosinetriphosphatase in the chicken after chronic dietary exposure

Recent work has shown that V accumulates in the kidney and is a potent inhibitor of Na+, K+‐adenosinetriphosphatase (ATPase) in vitro. Thus, as a nutritionally required element, V may regulate cation transport. The effect of chronic intake of the metal on Na+, K+‐A TPase in vivo has not been reported. In this study laying strain chickens were fed calcium orthovanadate for 15 mo from d 1 of age at levels of 0, 25, 50, and 100 ppm in the diet. Whole tissue homogenates and 13,000 × g fractions were analyzed for A TPase activities. Concentrations of V producing 50% inhibition of Na+, K+‐ATPase activity ranged from 1.0 × 10−5 M In liver to 1.8 × 10−6 M in kidney, which was the most sensitive tissue tested in vitro. Mg2+ ‐A TPase was more resistant to V than Na+, K+‐A TPase. Studies in vivo suggested a V‐dependent inhibition of renal Na+, K+‐ATPase. Correlation of enzyme specific activity and levels of V in kidneys suggested V‐A TPase mediated alteration in renal function.