Abstract
In order to elucidate the mechanism of action of glycyrrhetinic acid in causing the mineralocorticoid excess syndrome, the effect of the agent on the active transport of sodium in frog skin was examined. The rate of active transport was evaluated by a short circuit current using a Ussing's chamber. The short circuit current increased significantly after the addition of 10(-8) M aldosterone to the incubation media. It remained unchanged or suppressed when either glycyrrhizin or glycyrrhetinic acid was added. The addition of 10(-6) M glycyrrhetinic acid in the presence of 10(-8) M aldosterone stimulated the short circuit current significantly as compared with the control skin which was treated with aldosterone alone. From these results, glycyrrhetinic acid is thought to potentiate the action of aldosterone and facilitate the active transport of sodium in amphibian epithelium. It is suggested that the pseudoaldosteronism induced by the administration of glycyrrhizin in man may in part be due to the potentiation of aldosterone action by this drug.
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