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.