11β-羟化类固醇脱氢酶与高血压  

11β-hydroxysteroid dehydrogenase and hypertention

作　　者：姚兵[1] 张银娣[1] 

机构地区：[1]南京医科大学临床药理研究所,南京210029

出　　处：《中国药理学通报》2001年第6期617-620,共4页Chinese Pharmacological Bulletin

摘　　要：11β 羟化类固醇脱氢酶 (11β HSD)催化氢化可的松和可的松的相互转化 ,11β HSD2活性先天性缺陷引起表观盐皮质激素过多综合症 (AME) ,甘草等物质可抑制此酶活性引起AME样症状。 11βhydroxysteroid dehydrogenase (11β HSD) catalyzes the interconversion of cortisol with its inactive metabolite cortisone. The congenital deficiency of 11β HSD2 induce hypertension and hypokalemia. This disorder is called 'Apparent Mineralocorticoid Excess(AME)'. Glycyrrhizic acid and other endo and xenobiotics have been found to inhibit the activity of 11β HSD and cause excess mineralocorticoid effects that is similar to AME. The decrease in 11β HSD activity is related with the acquired and congenital hypertention.

关 键 词：11β-羟化类固醇脱氢酶 皮质激素过多综合症 高血压 AME 病因 

分 类 号：Q55[生物学—生物化学]