Aggregation of carp (Cyprinus carpio) thrombocytes, in comparison with that of rat platelets, was studied by the whole blood method using an impedance aggregometer. Carp thrombocyte aggregation, much like that of rat platelets, was triggered by collagen. Adenosine 5’-diphosphoric acid (ADP) caused rat platelet aggregation but failed to induce carp thronibocyte aggregation. While arachidonic acid effectively induced rat platelet aggregation, carp thrombocytes did not respond to the addition of arachidonic acid in 3 out of 4 cases. These findings show differences in aggregation behaviors, in response to various aggregating agents, between rat platelets and carp thrombocytes. The aggregating responses of rat platelets and carp thrombocytes induced by collagen were inhibited by indomethacin, a typical cyclooxygenase inhibitor. This raised the possibility of prostaglandin (s) involvement in the mechanism of carp thrombocyte aggregation, in a manner similar to that in rat platelets. Thrombocyte aggregation, induced in the carp by collagen, was inhibited by stable prostacyclin (PGI_2) analogues (Iloprost and Beraprost), 3 -isobutyl-1 -methylxanthine (phosphodiesterase inhibitor) and N^6, O^2-dibutyryl adenosine 3’： 5’-cyclic monophosphoric acid (db-cAMP), as similar to that of rat platelet aggregation. These results raised the possibility of cyclic AMP (cAMP) involvement in the mechanism of carp thrombocyte aggregation, in a manner similar to that, in rat platelets. Thrombocyte aggregation, induced in the carp by collagen, failed to be inhibited by sodium nitroprusside (SNP), a typical nitric oxide (NO) releaser, while SNP partially but significantly inhibited collagen-induced platelet aggregation in the rat. This suggests that NO/cyclic GMP (cGMP) does not play an inhibitory role in the mechanism of carp thrombocyte aggregation, unlike the aggregation in rat platelets.