The enhancement of prostacyclin (PGI2) formation in the cardiac and renal vessel wall by nafazatrom (BAY g 6575) and the vascular effects of this drug were studied in a series of experiments on perfused isolated rat hearts and kidneys. A dose-dependent increase of prostacyclin release (measured as 6-Keto-PGF1 alpha levels, delta % of control) from the vascular endothelium was achieved when nafazatrom was applied in concentrations ranging from 5 X 10(-7) to 10(-5) g/ml. In the heart, the minimal effective dose of nafazatrom was 5 X 10(-7) g/ml causing a 23 delta % increase of PGI2 release; maximal stimulation of PGI2 was 276 delta % at 5 X 10(-6) g/ml nafazatrom. In the kidney, only at the highest concentration of 10(-5) g/ml an increase of PGI2 to 192 delta % was found. Concomitant to the PGI2 release, in both organs, a reduction of perfusion pressure (delta % of control) was observed. Minimal vasodilation in the heart was - 9.6 delta % (5 X 10(-6) g/ml nafazatrom); the maximal effect was - 25.7 delta % (5 X 10(-6) g/ml nafazatrom). In the kidney, the only observed reduction of perfusion pressure was - 12 delta % at 10(-5) g/ml nafazatrom. The cyclooxygenase inhibitor indomethacin (10(-5) g/ml) blocked vasodilation produced by nafazatrom (5 X 10(-6) g/ml); delta P % was 0.5 + 1.