Abstract

The stimulation of Na + transport in the toad bladder by aldosterone is associated with an increased utilization of oxygen and an increase in the evolution of 14CO 2 from [6- 14C]glucose in response to the increased energy requirement of stimulated Na + transport. These are secondary effects of aldosterone and are abolished by the removal of Na + from the mucosal bathing medium and consequent absence of Na + transport. At the same time, however, aldosterone decreases the evolution of 14CO 2 from [1- 14C]glucose. This effect persists even in the absence of Na + and has similar characteristics of time of onset, concentration response, steroid specificity, and sensitivity to actinomycin D and spirolactone. Both the effect of aldosterone to decrease the evolution of 14CO 2 from [1- 14C]-glucose and its ability to stimulate Na + transport can be reproduced by adenosine 3′,5′-phosphate (cyclic AMP). This has been shown for endogenous cyclic AMP produced by the action of theophylline or vasopressin in combination with theophylline and for exogenous cyclic AMP as seen with N 6-2′- O-dibutyryl adenosine 3′,5′-phosphate (dibutyryl cyclic AMP) or with cyclic AMP in the presence of low concentrations of theophylline. Although these results suggest that cyclic AMP might mediate the action of aldosterone, no change in tissue concentration of cyclic AMP was found even after prolonged incubation with the hormone.

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