Influence of calcium-channel blockers on platelet function and arachidonic acid metabolism.
Available data indicate that platelet function and arachidonic acid metabolism are important factors in hemostasis and regulation of vascular tone. Plasma membrane and intracellular mobilization of calcium ions are intimately related to platelet activation and release of platelet contents. Release of arachidonic acid from membrane phospholipids as well as subsequent synthesis and release of vasoconstrictor thromboxane A2 are also regulated by movement of calcium ions. Adenosine 3':5'-cyclic phosphate in turn controls levels of free calcium ions in platelets and regulates calcium-dependent reactions. Slow-channel calcium blockers, such as verapamil, diltiazem and nifedipine, inhibit platelet activation in vitro, and decrease platelet adhesion intravascularly. These agents have also been shown to decrease platelet nucleotide release and thromboxane A2 generation. Some preliminary data suggest that calcium blockers also increase generation of vasodilator and platelet antiaggregant prostacyclin, which could contribute to decrease in platelet function. These effects of calcium blockers on platelet function and arachidonic acid metabolism could contribute in part to their efficacy in patients with ischemic heart disease.
Mehta
J L
JL
D000818:Animals; D001095:Arachidonic Acids / Q000097:blood*; D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D002118:Calcium / Q000097:blood / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D000242:Cyclic AMP / Q000502:physiology; D004110:Diltiazem / Q000494:pharmacology; D004285:Dogs; D004347:Drug Interactions; D006801:Humans; D009543:Nifedipine / Q000494:pharmacology; D010974:Platelet Aggregation / Q000187:drug effects; D014700:Verapamil / Q000494:pharmacology
D001095:Arachidonic Acids; D002121:Calcium Channel Blockers; D014700:Verapamil; D000242:Cyclic AMP; D004110:Diltiazem; D009543:Nifedipine; D002118:Calcium