Inhibition of platelet function of antiarrhythmic drugs, verapamil and disopyramide.
Various cardiovascular drugs such as nitrates and propranolol, used in the treatment of coronary artery disease have been shown to have an antiplatelet effect. We have studied the in vitro effects of two antiarrhythmic drugs, verapamil and disopyramide, and have shown their inhibitory effect on platelet function. Verapamil, a calcium channel blocker, inhibited the second phase of platelet aggregation induced by adenosine diphosphate (*ADP) and inhibited aggregation induced by collagen. Disopyramide similarly inhibited the second phase of platelet aggregation caused by ADP and aggregation induced by collagen. Either drug in synergism with propranolol inhibited ADP or collagen-induced platelet aggregation. Disopyramide at high concentrations inhibited arachidonic acid whereas verapamil was without effect. Verapamil, but not disopyramide, inhibited aggregated induced by the ionophore A23187.
D000255:Adenosine Triphosphate / Q000378:metabolism; D001095:Arachidonic Acids / Q000378:metabolism; D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism; D003327:Coronary Disease / Q000188:drug therapy; D004206:Disopyramide / Q000494:pharmacology*; D006801:Humans; D010974:Platelet Aggregation / Q000187:drug effects; D011433:Propranolol / Q000494:pharmacology; D011725:Pyridines / Q000494:pharmacology*; D013929:Thromboxane B2 / Q000096:biosynthesis; D014700:Verapamil / Q000494:pharmacology*
D001095:Arachidonic Acids; D011725:Pyridines; D013929:Thromboxane B2; D000255:Adenosine Triphosphate; D011433:Propranolol; D014700:Verapamil; D004206:Disopyramide