NA-K ACTIVATED ADENOSINE TRIPHOSPHATASE AND SODIUM TRANSPORT IN TOAD BLADDER.

Abstract

The effect of several agents in vitro on sodium transport by the intact toad bladder and on sodium-potassium activated, magnesium-dependent ATPase (Na-K ATPase) activity has been examined in an attempt to elucidate the relationship between the agents, the Na-K ATPase system, and active sodium transport. Ouabain and erythrophleine inhibited sodium transport and Na-K ATPase activity, but had no effect on sodium-potassium independent, magnesium-dependent ATPase (Mg-ATPase) activity. Vasopressin, adenosine 3',5'-monophosphate (cyclic-AMP), and aldosterone had no effect on Na-K ATPase or Mg-ATPase activity. The results are compatible with the assumption that the Na-K ATPase system is closely related to the active sodium pump, and that ouabain and erythrophleine inhibit sodium transport by the bladder through inhibition of the Na-K ATPase system. The stimulatory effect on sodium transport of vasopressin, cyclic-AMP, and aldosterone is not due to direct stimulation of the Na-K ATPase system.