Zhang Y D, Lorenzo B, Reidenberg M M
Department of Pharmacology, Cornell University Medical College, New York, NY 10021.
J Steroid Biochem Mol Biol. 1994 May;49(1):81-5. doi: 10.1016/0960-0760(94)90304-2.
Inhibition of 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) can cause excess mineralocorticoid effects and hypokalemia. Several substances causing hypokalemia (glycyrrhizic acid in licorice and gossypol) inhibit this enzyme. We tested other compounds for activity to inhibit 11 beta-OHSD in guinea pig kidney cortex microsomes with NADP as cofactor and cortisol as substrate. Furosemide was an inhibitor while bumetanide was not, indicating a mechanism for the increase K+ excretion caused by furosemide compared with bumetanide. Naringenin (found in grapefruit juice), ethacrynic acid, and chenodeoxycholic acid had inhibitor IC50 values similar to glycyrrhizic acid. We conclude that various compounds can inhibit this enzyme and may play a role in K+ metabolism and adrenocorticosteroid action.
抑制11β-羟类固醇脱氢酶(11β-OHSD)可导致盐皮质激素作用过度和低钾血症。几种可引起低钾血症的物质(甘草中的甘草酸和棉酚)可抑制该酶。我们以NADP为辅因子、皮质醇为底物,在豚鼠肾皮质微粒体中测试了其他化合物抑制11β-OHSD的活性。呋塞米是一种抑制剂,而布美他尼不是,这表明与布美他尼相比,呋塞米导致钾排泄增加的机制。柚皮苷(存在于葡萄柚汁中)、依他尼酸和鹅去氧胆酸的抑制剂IC50值与甘草酸相似。我们得出结论,各种化合物均可抑制该酶,并可能在钾代谢和肾上腺皮质类固醇作用中发挥作用。