Thromb Haemost 1981; 45(02): 158-161
DOI: 10.1055/s-0038-1650155
Original Article
Schattauer GmbH Stuttgart

Inhibition of Human Platelet Functions by Verapamil

Y Ikeda
The Department of Hematology, Keio University, School of Medicine, Tokyo, Japan
,
M Kikuchi
The Department of Hematology, Keio University, School of Medicine, Tokyo, Japan
,
K Toyama
The Department of Hematology, Keio University, School of Medicine, Tokyo, Japan
,
K Watanabe
*   Department of Clinical Pathology, Keio University, School of Medicine, Tokyo, Japan
,
Y Ando
*   Department of Clinical Pathology, Keio University, School of Medicine, Tokyo, Japan
› Institutsangaben
Weitere Informationen

Publikationsverlauf

Received 02. April 1980

Accepted after revision 05. Februar 1981

Publikationsdatum:
05. Juli 2018 (online)

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Summary

The effects of verapamil, a coronary vasodilator, on platelet functions were studied.

Platelet aggregation induced by ADP, epinephrine or collagen was inhibited by verapamil in vitro. Calcium ionophore A23187-induced platelet aggregation was also inhibited by verapamil in a concentration dependent manner. In washed platelets, verapamil caused a dose-dependent inhibition of serotonin release induced either by thrombin or A23187 in the absence of extracellular calcium. Addition of 1 mM CaCl2 with A23187 or thrombin partially overcame this inhibition. Addition of 1 mM CaCl2 in the absence of verapamil had no effect on thrombin- or A23187-induced secretion. When verapamil was administered to the healthy volunteers at the dosage commonly used, inhibition of platelet aggregation was observed 2 hrs after the drug ingestion. It is of great interest that verapamil potentiated the anti-aggregating activity of prostacyclin in vitro.

Our results may suggest a potential role for verapamil in the treatment of thrombotic disorders.