The effect of aldosterone on Na entry and Na exit from the toad urinary bladder epithelium was studied using current-voltage analysis of the apical cell membrane to measure apical Na permeability (PNa) and the intracellular Na activity (Nac). Varying the activity of Na in the mucosal solution elicited parallel changes in active Na transport (INa) and Nac, allowing the activation of the basolateral Na pump by Nac to be evaluated. Five hours after addition of aldosterone, INa increased 130% and PNa increased 140% relative to controls. The pump rate at an arbitrarily chosen value of Nac = 4 mM [Ip(4)] increased 53%. Eighteen hours after addition of the hormone, INa increased 500%, PNa increased 680%, and Ip(4) increased 110%. ADH increased INa and PNa without changing Ip(4), whereas KCN decreased all three parameters. A change in the activation curve for the pump induced by aldosterone was also observed in the presence of mucosal nystatin, which permeabilized the apical membrane, allowing Nac to be controlled. Attempts to distinguish an effect on the maximal pump rate from one on the affinity for Na were equivocal. The results imply that aldosterone has independent stimulatory effects on Na entry across the apical membrane and Na exit across the basolateral membrane but that the stimulation of the entry process is considerably stronger.