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The effects of nifedipine, a calcium antagonist, on platelet function
Insights
Nifedipine, a calcium antagonist, moderately reduced platelet aggregation and prolonged bleeding time in patients with coronary heart disease. This suggests nifedipine may inhibit calcium transport in platelets.
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Hematology
Background:
- Coronary heart disease (CHD) involves complex cardiovascular processes.
- Platelet function plays a critical role in thrombotic events associated with CHD.
- Calcium ions are essential for platelet activation and aggregation.
Purpose of the Study:
- To investigate the effects of nifedipine, a novel calcium antagonist, on platelet function in patients with CHD.
- To assess changes in platelet aggregation, adhesiveness, and bleeding time following nifedipine administration.
Main Methods:
- Studied 20 patients with coronary heart disease before and 1 hour after a single 20 mg dose of nifedipine.
- Measured platelet counts, platelet adhesiveness (Hellem's method), and platelet aggregation (adenosine diphosphate and collagen-induced).
- Assessed mean bleeding time after nifedipine ingestion.
Main Results:
- Nifedipine did not significantly alter platelet counts or adhesiveness.
- A significant reduction (20-26%) in maximal platelet aggregation rate induced by adenosine diphosphate was observed.
- Collagen-induced platelet aggregation decreased by 23%, and mean bleeding time increased by 12% (36 seconds).
Conclusions:
- Nifedipine exerts a moderate inhibitory effect on platelet aggregation in patients with CHD.
- The observed effects on platelet function and bleeding time suggest nifedipine may inhibit calcium transport across platelet membranes.
- These findings indicate a potential antiplatelet effect of nifedipine, possibly contributing to its cardiovascular benefits.
Abstract:
Platelet function was studied before and 1 hour after ingestion of 20 mg nifedipine, a new calcium antagonist, in 20 patients with coronary heart disease. Platelet counts remained unchanged. Platelet adhesiveness, measured as retention in glass bead columns with Hellem's method for native blood, did not drop significantly eigher when 0.9 or 3.6 ml of blood was used. Platelet aggregation, which is dependent on extracellular calcium, was induced in citrated platelet-rich plasma. The mean maximal rate of primary aggregation, initiated with three different concentrations of adenosine diphosphate, was reduced by 20% to 26%. The rate of irreversible collagen-induced aggregation was on average 23% lower after nifedipine. The mean bleeding time was 36 seconds, or 12%, longer after ingestion of the drug. The moderate, but significant reduction of platelet aggregation and prolongation of the bleeding time by nifedipine may be mediated through inhibition of calcium transport across the platelet membrane.