AJP - Renal Physiology, Vol 244, Issue 2 105-F111, Copyright © 1983 by American Physiological Society
Vanadium, Na-K-ATPase, and potassium adaptation in the rat
H. Higashino, J. D. Bogden, M. A. Lavenhar, J. W. Bauman Jr, T. Hirotsu and A. Aviv
Vanadate is a potent inhibitor of Na-K-ATPase in vitro. It has been
suggested that vanadium may function as a cellular regulator of Na-K-ATPase
in vivo. To examine this speculation, we studied in rats the effect of high
vanadate intake on 1) the tissue levels and distribution of vanadium, 2)
basal activity of Na-K-ATPase in various tissues, and 3) the activity of
Na-K-ATPase in various organs under conditions of massive chronic potassium
loading known to stimulate Na-K-ATPase in the kidney and colon. Despite
extremely high tissue levels of vanadium there was no demonstrable effect
of the element on the basal activity of Na-K-ATPase. When subjected to
chronic potassium loading, rats with high tissue vanadium concentrations
underwent potassium adaptation that was associated with a rise in
Na-K-ATPase activity in the renal cortex, renal medulla, and colonic
mucosa. Further studies are needed to support or refute the thesis that
vanadium might be an intracellular regulator of Na-K-ATPase in vivo.
