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The Effect of Aldosterone on Glycolysis in the Urinary Bladder of the Toad

From the ¹ From the Laboratory of Kidney and Electrolyte Metabolism, National Heart Institute, National Institutes of Health, Bethesda, Maryland 20014

Prolonged incubation with aldosterone causes an increase in the rate of sodium transport and in the rate of glycolysis in the urinary bladder of the toad (Bufo marinus) in vitro. When sodium transport was inhibited by ouabain after the effect of aldosterone was manifest, the rate of sodium transport as well as the rate of glycolysis fell to the same low value in aldosterone-treated tissue and in paired control tissue that had been incubated without hormone. When bladders were made anaerobic after the aldosterone effect was manifest, short circuit current fell in both preparations, but remained significantly higher in aldosterone-treated tissue than in paired control tissue. During anaerobiosis, the rate of lactate production was higher in aldosterone-treated tissue than in paired anaerobic control tissue. Thus the effect of aldosterone on glycolysis appears to be related to its effect on sodium transport and does not depend entirely upon oxidative metabolism. Measurement of the concentration of glycolytic intermediates and cofactors in tissue incubated with aldosterone indicated activation of phosphofructokinase and pyruvate kinase. There was no change in the concentration of adenosine mono-, di-, or triphosphate, or inorganic phosphate, but there was a fall in creatine phosphate and a rise in the concentration of creatine in aldosterone-treated tissue. This pattern is interpreted as indicating that the stimulation of sodium transport by aldosterone (or an aldosterone-induced protein) is a direct effect on sodium transport and not secondary to an effect of the hormone on energy production.

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