Ishikawa S, Saito T
Endocrinol Jpn. 1980 Dec;27(6):697-701. doi: 10.1507/endocrj1954.27.697.
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.
为阐明甘草次酸导致盐皮质激素过多综合征的作用机制,研究了该药物对蛙皮钠主动转运的影响。采用Ussing氏槽通过短路电流评估主动转运速率。向孵育培养基中添加10(-8)M醛固酮后,短路电流显著增加。添加甘草酸或甘草次酸时,短路电流保持不变或受到抑制。与仅用醛固酮处理的对照皮肤相比,在存在10(-8)M醛固酮的情况下添加10(-6)M甘草次酸可显著刺激短路电流。根据这些结果,认为甘草次酸可增强醛固酮的作用并促进两栖类上皮细胞中钠的主动转运。提示人类服用甘草酸所致的假性醛固酮增多症可能部分归因于该药物对醛固酮作用的增强。