Abstract
The aim of this study was to examine whether therapeutical doses of nitrendipine influence platelet function. In eight healthy subjects, the platelet aggregation response to collagen in whole blood and platelet-rich plasma (PRP) was monitored over 12 h after single administration of 40 mg nitrendipine given orally and was strongly inhibited between 60-83% (0.3 microgram/ml collagen) versus baseline at the third and fourth hour. Stimulated thromboxane formation from exogeneous arachidonic acid decreased almost continuously, with lowest levels at the 12th hour. Basal thromboxane remained below 25 pg/ml, but platelet factor 4 increased to more than twice the baseline level in the fourth hour, presumably reflecting adrenergic counterregulation of hypotensive effects. These preliminary data show that therapeutic drug concentrations of nitrendipine inhibit platelet function. Therefore, calcium channel blockers may be of therapeutical value in the treatment of prethrombotic states with primary platelet hyperactivity as present, for example, in diabetes mellitus.
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