The purpose of this research was to test whether the positive inotropic and antiarrhythmic effects of bradykinin are due solely to increases in coronary flow. Rat hearts were perfused at constant pressure (75 cm H2O) and temperature (37 degrees C). Coronary flow was measured using an electronic drop counter. Contractile force was assessed using a left ventricular balloon catheter. Bradykinin (10 nmol/L) significantly increased coronary flow by 55 +/- 8% above the control level of 4.8 +/- 0.5 mL/min (n = 20), while force was increased by 23.1 +/- 3% (n = 20). Ramiprilat (10 nmol/L) potentiated the vasodilatory and inotropic responses to 10 nmol/L bradykinin by 58 +/- 8% (n = 5). When hearts were perfused at constant flow, bradykinin no longer produced a positive inotropic effect. Bradykinin, 10 or 100 nmol/L, under these conditions actually caused a negative inotropic effect of -24.8 +/- 5% (n = 8) and -35 +/- 11% (n = 3), respectively. In another 2 groups of hearts, also perfused at constant pressure, reperfusion arrhythmias were elicited after a 20-min period of complete global ischemia. In control hearts, the mean period of fibrillation was 7.3 +/- 1.8 min (n = 10). This period was significantly reduced to 2.7 +/- 0.7 min (n = 10) in hearts receiving 10 nmol/L bradykinin. In untreated hearts, the coronary flow during the reperfusion period increased over the baseline flow by a factor of 1.8 +/- 0.2, and this factor was not significantly effected by bradykinin. These results suggest that only the positive inotropic, but not the antiarrhythmic, action of bradykinin is due to coronary vasodilation.