Someya N, Morotomi Y, Kodama K, Kida O, Higa T, Kondo K, Tanaka K
J Cardiovasc Pharmacol. 1984 Sep-Oct;6(5):840-3. doi: 10.1097/00005344-198409000-00016.
Effects of captopril on platelet aggregation were studied in 12 essential hypertensive subjects. At the same time, the effects of captopril and angiotensin II on platelet aggregation in vitro were examined in 20 volunteers. A 50-mg oral dose of captopril was administered daily to hypertensive subjects for 2 weeks; the dose was then increased to 100 mg daily for the next 2 weeks. Values of platelet aggregation induced by ADP, epinephrine, collagen, and arachidonic acid before captopril treatment were 71.9 +/- 4.5, 77.3 +/- 4.2, 72.4 +/- 4.1, and 70.8 +/- 4.3% (mean +/- SE), respectively. Two weeks after daily administration of 50 mg captopril, these values were 56.7 +/- 4.5, 50.8 +/- 7.6, 64.0 +/- 4.6, and 60.9 +/- 3.9%, respectively, with significant reduction of platelet aggregation (p less than 0.001, p less than 0.01, p less than 0.01, and p less than 0.005, respectively). Daily administration of 100 mg captopril also had a significant suppressive effect on platelet aggregation. Changes of platelet count and serum lipids were not significant. In vitro, captopril and angiotensin II added to platelet-rich plasma had no effect on platelet aggregation. These results show that the suppressive effect of captopril on platelet aggregation is a secondary action in vivo.