Shepherd A N, Campbell B C, Reid J L
J Cardiovasc Pharmacol. 1982 May-Jun;4(3):381-7. doi: 10.1097/00005344-198205000-00007.
Captopril (SQ 14 225) was administered to normotensive, sodium-replete volunteers in order to investigate the relationships between its haemodynamic effects and effects on sympathetic activity, the renin-angiotensin-aldosterone system, and plasma-converting enzyme activity. Following the administration of captopril (25 mg) orally, mean arterial pressure fell (supine 89.1 +/- 5.9 to 81.1 +/- 3.3 mm Hg, p less than 0.01; erect 98.5 +/- 5.5 to 87.4 +/- 6.7 mm Hg, p less than 0.01) but heart rate did not change. Plasma noradrenaline rose; plasma renin activity and angiotensin I concentration rose, while angiotensin II and aldosterone fell; plasma-converting enzyme was inhibited for 6 h. The extent of blood pressure reduction and converting enzyme inhibition was closely correlated (r = 0.92, p less than 0.001). Plasma captopril concentration was directly related to converting enzyme inhibition in an in vitro study using plasma from the same subjects. In the absence of a convenient assay of captopril, converting enzyme may be used as an index of captopril concentration in the further study of kinetic and dynamic relationships.
为了研究卡托普利（SQ 14 225）的血流动力学效应与对交感神经活性、肾素 - 血管紧张素 - 醛固酮系统及血浆转换酶活性的影响之间的关系，对血压正常、钠负荷充足的志愿者给予卡托普利。口服卡托普利（25毫克）后，平均动脉压下降（仰卧位从89.1±5.9降至81.1±3.3毫米汞柱，p<0.01；站立位从98.5±5.5降至87.4±6.7毫米汞柱，p<0.01），但心率未改变。血浆去甲肾上腺素升高；血浆肾素活性和血管紧张素I浓度升高，而血管紧张素II和醛固酮降低；血浆转换酶被抑制达6小时。血压降低程度与转换酶抑制程度密切相关（r = 0.92，p<0.001）。在一项使用相同受试者血浆的体外研究中，血浆卡托普利浓度与转换酶抑制直接相关。在缺乏便捷的卡托普利检测方法时，在进一步研究动力学和动态关系时，转换酶可用作卡托普利浓度的指标。
