血管紧张素转换酶（ACE）结合位点饱和对依那普利拉人体药代动力学的影响。

The effect of saturation of ACE binding sites on the pharmacokinetics of enalaprilat in man.

Wade J R, Meredith P A, Hughes D M, Elliott H L

Department of Medicine and Therapeutics, University of Glasgow, Gardiner Institute, Western Infirmary.

Br J Clin Pharmacol. 1992 Feb;33(2):155-60. doi: 10.1111/j.1365-2125.1992.tb04018.x.

Eight healthy male volunteers received oral enalapril, 10 mg, in the presence and absence of pretreatment with captopril, 50 mg, twice daily for 5 days. 2. Enalaprilat pharmacokinetics were characterised after both doses of enalapril to investigate the effect of saturating ACE binding sites by pretreatment with captopril. 3. The pharmacokinetics of enalaprilat were best described by a one compartment model with zero order input incorporating saturable binding to plasma and tissue ACE. 4. Values of AUC (0.72 h) for enalaprilat were 419 +/- 97 and 450 +/- 87 ng ml-1 h in the presence and absence of captopril, respectively. The difference was not statistically significant nor were there any other differences in model parameters. 5. Induction of ACE by captopril resulting in an increase in the number of ACE binding sites, may have obscured any effect of captopril on the occupancy of ACE binding sites by enalapril.

八名健康男性志愿者在每日两次服用50毫克卡托普利预处理5天的情况下以及未进行预处理的情况下，分别口服10毫克依那普利。
分别给予两种剂量的依那普利后，对依那普利拉的药代动力学进行了表征，以研究通过卡托普利预处理使血管紧张素转换酶（ACE）结合位点饱和的影响。
依那普利拉的药代动力学最好用一个零级输入的单室模型来描述，该模型包含与血浆和组织ACE的饱和结合。
有卡托普利预处理和无卡托普利预处理时，依那普利拉的AUC（0.72小时）值分别为419±97和450±87纳克/毫升·小时。差异无统计学意义，模型参数也无其他差异。
卡托普利诱导ACE导致ACE结合位点数量增加，可能掩盖了卡托普利对依那普利占据ACE结合位点的任何影响。

The effect of saturation of ACE binding sites on the pharmacokinetics of enalaprilat in man.