Thromb Haemost 1983; 50(02): 513-517
DOI: 10.1055/s-0038-1665243
Original Article
Schattauer GmbH Stuttgart

Effect of the Calcium-Entry Blocking Agent Nifedipine on Activation of Human Platelets and Comparison with Verapamil

P Han
The Department of Medicine and Clinical Science, The John Curtin School of Medical Research, The Australian National University, Canberra, ACT, Australia
,
C Boatwright
The Department of Medicine and Clinical Science, The John Curtin School of Medical Research, The Australian National University, Canberra, ACT, Australia
,
N G Ardlie
The Department of Medicine and Clinical Science, The John Curtin School of Medical Research, The Australian National University, Canberra, ACT, Australia
› Author Affiliations
Further Information

Publication History

Received 17 December 1982

Accepted 05 May 1983

Publication Date:
18 July 2018 (online)

Summary

The effects of the calcium-entry blocking agent nifedipine on the activation of human platelets by various agonists has been studied and compared with verapamil. Like verapamil, nifedipine inhibited platelet aggregation and secretion caused by collagen, the second phase of ADP-induced aggregation, and aggregation caused by the ionophore A23187. Both agents inhibited the formation of TXB2 from endogenous arachidonate, whereas only nifedipine inhibited platelet aggregation and decreased TXB2 formation caused by exogenous arachidonate without inhibiting uptake. These results indicate that both calcium-blocking agents may be inhibiting the release of arachidonate in platelets by phospholipases, and that nifedipine also inhibits the formation and action of thromboxane A2 in platelets. Epinephrine-induced aggregation was inhibited by low concentrations of verapamil while nifedipine only inhibited aggregation by epinephrine at much higher concentrations. It is suggested that low concentrations of verapamil inhibit epinephrine-induced aggregation by interacting with platelet α-adrenergic receptors, and that higher concentrations of both calcium-blocking agents inhibit platelet responses to other aggregating agents by preventing intracellular calcium mobilization.

 
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