探讨棉酚诱发低钾血症机制．方法：从豚鼠肾脏皮质制备１１βＯＨＳＤ，反相高效液相测定该酶活性．结果：依赖辅酶Ｉ的１１βＯＨＳＤ的Ｖｍａｘ＝０６４ｍｍｏｌ·ｈ－１／ｇｐｒｏｔｅｉｎ，Ｋｍ＝００７μｍｏｌ；依赖辅酶ＩＩ的１１βＯＨＳＤ的Ｖｍａｘ＝１７５ｍｍｏｌ·ｈ－１／ｇｐｒｏｔｅｉｎ，Ｋｍ＝０２１μｍｏｌ．棉酚对它们的抑制有显著差异，ＩＣ５０（９５％可信限）前者为５０２（４８３－５２０）μｍｏｌ，后者为１１４３（１０９８－１１８８）μｍｏｌ，抑制常数Ｋｉ分别为９６ｍｍｏｌ·Ｌ－１和３４０ｍｍｏｌ·Ｌ－１．结论：抑制依赖辅酶Ｉ的１１βＯＨＳＤ是棉酚诱发低钾血症的更主要的生理因素． Explore gossypol-induced hypokalemia mechanism. Methods: 11β-OHSD was prepared from the cortex of guinea pig kidney and the enzyme activity was determined by RP-HPLC. Results: Vmax = 064mmol · h-1 / gprotein and Km = 007μmol in 11β-OHSD dependent on coenzyme I; Vmax = 1175 mmol · h-1 / gprotein in coenzyme II-dependent 11β-OHSD with Km = 0  21μmol. The inhibition of gossypol was significantly different with IC50 (95% confidence limit) of 502 (483-520) μmol, and the latter of 1143 (1098-1188) μmol. The inhibition constants Ki were 96mmol·L-1 and 340mmol·L-1. CONCLUSIONS: Inhibition of 11β-OHSD that is dependent on coenzyme I is a more important physiological factor for gossypol-induced hypokalemia.