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A series of synthetic analogues of prostacyclin (PGI2) have been compared for their ability to increase the formation of cyclic AMP and to inhibit the aggregation of human platelets, and for relaxation of isolated bovine coronary arteries and lowering of the blood pressure of concious rats. The most active inhibitors of aggregation were derivatives of PGI2 with a triple bond at C14:15. There was good aggreement between the inhibition of platelet aggregation and elevation of cyclic AMP in platelets, and both effects were enhanced by phosphodiesterase inhibitors. The most active compounds of the series were K13415 (14,15-didehydro 20-methyl PGI2), and a carbocyclic analog, FCE21258 (5e-14,15-didehydro carbo PGI2) which were both more active than PGI2 itself. In addition, the carbocyclic compounds were stable at neutral pH. Compounds K13817 (14,15-didehydro 16-methyl PGI2) and FCE21292 (5e-14,15 didehydro 20-methyl carbo PGI2) were similar in activity to PGI2 as platelet inhibitors, but had less vasodilator and depressor activity. The results show considerable differences in the structural specificities of the platelet and vascular activities of PGI2.

Vascular And Platelet Effects Of Synthetic Analogues Of Prostacyclin