The binding of concanavalin A (con A) to washed human platelets was demonstrated with [63Ni] and [3H] labeled preparations. When con A binding was inhibited by α-methyl-d-mannoside, the con A-induced platelet release reaction was inhibited. PGE1 markedly inhibited the release of nucleotides, serotonin and α-mannosidase (α-man) produced by both con A and thrombin but caused only a moderate decrease in con A binding. ATP, which inhibited release of serotonin by con A and thrombin, also caused a moderate decrease in con A binding. Amantadine, 5 mM, potentiated release of serotonin and most glycosidases from thrombin-treated platelets, but did not affect nucleotide or α-man release. Although 1 mM amantadine also enhanced serotonin release by con A-treated platelets without affecting release of nucleotides, 5 mM amantadine inhibited con A-stimulated release of serotonin, nucleotides and α-man and produced a 30 per cent reduction in con A binding. These data suggest that: (1) con A and thrombin activate release receptors by different mechanisms, (2) activation by con A may require binding to the receptors, (3) the mechanism for release after activation is similar for both, and (4) receptors governing the release of serotonin are different from those involved in release of nucleotides and α-man.
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