Abstract
Vanadium compounds have been reported to inhibit the (Na+ + K+)ATPase activity of several cell membrane preparations1–3, to have a positive inotropic effect on ventricular cardiac muscle4, slightly increase myocardial cyclic AMP levels5, stimulate fat cell adenylate cyclase6, and cause natriuresis in rats7. Recently we have reported that vanadate produces a transient, initial stimulation of (Na+ + K+) ATPase activity in a cat heart cell membrane preparation, in addition to its well known inhibitory action on this enzyme system8. The transient stimulation occurred at the same concentration range as did the inotropic effects. There was, however, a serious discrepancy between the time courses of the two events. The former lasted only a few minutes, whereas the latter remained virtually stable for at least 30 min. The supposed stimulatory action of vanadate on (Na+ + K+)ATPase was deduced from an initial rapid loss of NADH in the ATPase assay used (optical coupled assay with an ATP regenerating system9). The oxidation of NADH was followed photometrically by continuous recording8. We now report that the rapid loss of NADH and hence the claimed transient stimulatory action of high concentrations of vanadate on the (Na+ + K+)ATPase activity is caused rather by an oxidation of NADH as a result of a NADH-dependent reduction of vanadate.
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Erdmann, E., Krawietz, W., Philipp, G. et al. Purified cardiac cell membranes with high (Na+ + K+) ATPase activity contain significant NADH-vanadate reductase activity. Nature 282, 335–336 (1979). https://doi.org/10.1038/282335a0
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DOI: https://doi.org/10.1038/282335a0
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