Epinephrine and the Ca2+ ionophore A23187 synergistically induce platelet aggregation without protein kinase C activation.
Aspirin-pretreated, 32P-prelabeled, washed human platelets resuspended in a buffer containing apyrase and 2% plasma were exposed to epinephrine and the Ca2+ ionophore A23187. Epinephrine potentiated platelet aggregation (not secretion), the production of [32P]phosphatidic acid and myosin light chain phosphorylation induced by A23187. No phosphorylation of the 40 kDa protein, the substrate of protein kinase C, was observed. We conclude that G1-protein activation evoked by epinephrine and Ca2+ mobilization caused by A23187 represents a novel synergism for platelet aggregation and that protein kinase C activation, under these conditions is not needed for platelet aggregation.
Olbrich
C
C
Medizinische Klinik Innenstadt der Universität München, FRG.
Siess
W
W
D000001:Calcimycin / Q000494:pharmacology*; D004357:Drug Synergism; D004789:Enzyme Activation / Q000187:drug effects; D004837:Epinephrine / Q000494:pharmacology*; D006801:Humans; D010712:Phosphatidic Acids / Q000096:biosynthesis; D010766:Phosphorylation; D010974:Platelet Aggregation / Q000187:drug effects*; D011493:Protein Kinase C / Q000378:metabolism*
D010712:Phosphatidic Acids; D000001:Calcimycin; D011493:Protein Kinase C; D004837:Epinephrine