FCE 22509, 5-(Z,E)-13,14-didehydro-20-methyl-carboprostacyclin, a chemically stable prostacyclin (PGI2) derivative, was 3.5 times more potent than PGI2 in relaxing bovine coronary artery in vitro; unlike PGI2, it did not contract bovine coronary vein and it antagonized PGI2-induced contractions of the coronary vein. In vitro smooth muscle (guinea pig ileum and trachea and rat stomach strip) was contracted to a lesser extent than with PGI2. FCE 22509 was about five times less potent than PGI2 in deaggregating platelet clumps formed on rabbit Achilles tendon bathed with heparinized cat blood (ED50 = 7.6 and 1.6 mcg/kg i.v. respectively). In the conscious normotensive and spontaneously hypertensive rat FCE 22509 lowered mean systemic arterial pressure (MSAP) (ED25 = 11.5 and 4.8 mcg/kg i.v.) to a lesser extent than PGI2 (ED25 = 2.1 and 2.34 mcg/kg i.v.) and increased heart rate but not dose-dependently. Orally administered, FCE 22509 likewise reduced MSAP though at high dosages (ED30 = 1.33 and 1.02 mg/kg in normotensive and hypertensive rats). Heart rate (HR) was raised after i.v. and oral treatment but not dose-dependently. In the open-chest anaesthetized dog, FCE 22509, compared with PGI2 at the same three doses, 0.2, 0.4 and 0.8 mcg/kg i.v., lowered MSAP but its hypotensive effect was less pronounced than that of PGI2. Like PGI2, FCE 22509 did not modify HR (though PGI2 showed a tendency to a decrease and FCE 22509 seemed to increase this cardiovascular function) and mean pulmonary arterial pressure (MPAP) and likewise significantly reduced myocardial contractile force. After infusion of PGI2 and FCE 22509 0.2 mcg/kg i.v. for 15 min in the open chest anaesthetized cat, the ex-vivo ADP-induced inhibition of platelet aggregation was the same for both compounds. Unlike PGI2, which reduced MSAP and MPAP, FCE 22509 had no significant lowering effect on MSAP and MPAP.