Greater sensitivity to vanadate of rat renal relative to cardiac (Na+ + K+)-ATPase.

Vanadate (VO4(-3] produces a positive inotropic effect in rats and also promotes diuresis as well as natriuresis. Although the mechanism(s) of these effects is uncertain, in the kidney, VO4(-3) may act through inhibition of (Na+ + K+)-ATPase activity, whereas in the heart, other or additional mechanisms are likely. Under the assay conditions used in the present study, microsomal (Na+ + K+)-ATPase activities from rat kidney cortex and medulla were inhibited to a greater extent than was left ventricular (Na+ + K+)-ATPase activity over a range of VO4(-3) concentrations. The apparent dissociation constant for left ventricular (Na+ + K+)-ATPase (10.95 +/- 1.26 X 10(-7)M VO4(-3] was significantly greater than that of (Na+ + K+)-ATPase from the cortex (3.46 +/- 0.96 X 10(-7)M VO4(-3] or the medulla (3.32 +/- 0.7 X 10(-7)M VO4(-3), N = 6, P less than .05) whereas there were no significant differences between the effects of VO4(-3) on (Na+ + K+)-ATPase from the cortex and medulla. The greater inhibition by VO4, of (Na+ + K+)-ATPase from the cortex relative to that of the left ventricle, occurred over a range of Na+ and K+ concentrations, and K+ enhanced the inhibition by VO4(-3) to a greater extent for (Na+ + K+)-ATPase from the cortex than the left ventricle. These results suggest that renal (Na+ + K+)-ATPase is more sensitive than left ventricular (Na+ + K+)-ATPase to inhibition by VO4(-3) and would, therefore, be more likely to be modulated in vivo.