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Thromb Haemost 1986; 56(03): 308-310
DOI: 10.1055/s-0038-1661673
Original Article
Schattauer GmbH Stuttgart

Verapamil Inhibits Platelet Aggregation by a Calcium-Independent Mechanism

Giovanni Bonadonna
The Institute of Chemistry and Clinical Microscopy, University of Verona, Verona, Italy
,
Clara Lechi
The Institute of Chemistry and Clinical Microscopy, University of Verona, Verona, Italy
,
Paola Corradini
The Institute of Chemistry and Clinical Microscopy, University of Verona, Verona, Italy
,
Daniela Sinigaglia
The Institute of Chemistry and Clinical Microscopy, University of Verona, Verona, Italy
,
Piero De Togni
*   The Institute of General Pathology, University of Verona, Verona, Italy
,
Grzeskowiak Miroslawa
*   The Institute of General Pathology, University of Verona, Verona, Italy
› Author Affiliations
Further Information

Publication History

Received 06 May 1986

Accepted 01 September 1986

Publication Date:
18 July 2018 (online)

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Summary

We studied the inhibitory effects of the calcium channel blocker verapamil both on platelet aggregation and intracellular calcium [Ca2+]i in platelets loaded with a fluorescent indicator (quin 2).

The inhibitory effects of verapamil on the platelet aggregation response to both thrombin and ionomycin were seen to be clearly dissociated from the verapamil-induced inhibition of the [Ca2+]i increase produced by these agonists. Verapamil-induced inhibition of platelet aggregation was also obtained when using the “calcium-independent” agonist phorbol-myristate acetate (PMA). It may be deduced that a calcium-independent mechanism plays a role in verapamil-induced inhibition of platelet aggregation. We postulate that this mechanism may operate via a protein-kinase C pathway.

Key words

Verapamil - Intracellular calcium - Platelet aggregation - Thrombin - Ionomycin
 

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