Bradykinin potentiating peptide C (BPPC) inhibits angiotensin-converting enzyme and bradykinin-destroying plasma kinases. It is possible that BPPC contributes to the regulation of cardiovascular functions during hypertension. The effect of BPPC on cardiovascular functions has not been investigated. Therefore, we studied the probable effects of this peptide on coronary perfusion pressure, heart rate and contractile force in rat hearts. Isolated hearts were perfused under a constant flow with modified Krebs-Hanseleit solution and 1, 10 and 100 nM BPPC infused to the hearts. Coronary perfusion pressure, heart rate and left ventricular developed pressure, an index of myocardial contractile force, were measured. All the doses of BPPC caused a significant reduction in perfusion pressure and developed pressure (p<0.001 for all). One and 10 nM BPPC increased the heart rate (p<0.05 and p<0.01, respectively) but, 100 nM decreased significantly (p<0.001). From our study, there is sufficient evidence that BPPC possesses vasodilatory efficacy with a modest negative inotropic action. Low doses of BPPC may show tachycardic effect, whereas higher dose may exert bradycardic action.