Application of bradykinin to the exposed ventricular surface of the dog's heart produced reflex pressor effects and tachycardia, whereas application of nicotine evoked reflex hypotension and bradycardia. Prostacyclin (PGI2) or prostaglandin E2 (PGE2), when applied epicardially, had no effects by themselves but potentiated the reflex pressor changes to bradykinin; the depressor responses to nicotine were not changed. The potentiating effect of PGI2 was prompt but short-lived, whereas that of PGE2 was slow in onset but prolonged. The results suggest that PGI2, which is present in the pericardial fluid, may contribute to signalling of pain and reflex circulatory changes when kinin formation occurs during myocardial ischaemia or pericardial inflammation.