Effects of TRK-100, a stable prostacyclin analogue, on regulation of cyclic AMP metabolism in platelets

Abstract TRK-100 is a chemically stable analogue of prostacyclin and effective in inhibiting platelet aggregation when orally administered in experimental animals. In the present study we compared the potency of TRK-100 with those PGI 2 and PGE 1 to cause an activation of adenylate cyclase activity in rat and human platelet membranes. TRK-100 was half as effective as PGI 2 , and 10 times more effective than PGE 1 in both platelet membranes. TRK-100 also induced an activation of phosphodiesterase activity when directly added to intact platelets probably as a feedback mechanism of intracellular cAMP level like PGI 2 did. TRK-100 would mimic PGI 2 in the regulation of cAMP metabolism.