Objectives To investigate the influences of bradykinin (BK) on hemodynamics, left ventricular hypertrophy and interstitial collagen metabolism after myocardial infarction (MI) in rats and the contribution of BK in angiotensin-converting enzyme (ACE) inhibition therapy. Methods By means of hemodynamic measurements, morphometric study of myocyte hypertrophy and SDS-PAGE technique, the effects of enalapril (500 μg·kg-1·day-1), enalapril (500 μg·kg-1·day-1) with BK B2 receptor antagonist Hoe-140 (500 μg·kg-1·day-1), angiotensin II (AgII) type 1 (AT1) receptor antagonist losartan (3 mg·kg-1·day-1) on mean arterial pressure (MAP), left ventricular end-diastolic pressure (LVEDP), as well as maximum positive left ventricular pressure change (+dp/dtmax), V(m) n, collagen content and the ratio of type I to type Ⅲ collagen (Ⅰ/Ⅲ)of noninfarcted area were observed in rats after MI. Treatments were started on the 3rd day after MI and continued for another 28 days. Results Enalapril reduced LVEDP, V(m)n and collagen content as well as collagen Ⅰ/Ⅲ compared with the untreated MI group (P<0.05), and all of these effects of enalapril were partly blunted by concomitant treatment with hoe-140(P<0.05). Losartan was less effective than enalapril (P<0.05). However, three treatment groups had no significant differences in +dp/dtmax and had similar reductions in MAP compared with untreated MI group. Conclusions BK can improve cardiac function and prevent left ventricular hypertrophy with myocardial fibrosis independent of blood pressure. The mechanisms of ACEI are both blockade of AngⅡ formation and inhibition of BK degradation. Objectives To investigate the influences of bradykinin (BK) on hemodynamics, left ventricular hypertrophy and interstitial collagen metabolism after myocardial infarction (MI) in rats and the contribution of BK in angiotensin-converting enzyme (ACE) inhibition therapy. Methods By means of hemodynamic measurements , morphometric study of myocyte hypertrophy and SDS-PAGE technique, the effects of enalapril (500 μg · kg -1 day -1), enalapril (500 μg · kg -1 day -1) with BK B2 receptor antagonist Hoe-140 (500 μg · kg -1 · day -1), angiotensin II (AgII) type 1 (AT1) receptor antagonist losartan (3 mg · kg -1 day -1) on mean arterial pressure (MAP) Diastolic pressure (LVEDP), as well as maximum positive left ventricular pressure change (+ dp / dtmax), V (m) n, collagen content and the ratio of type I to type III collagen (Ⅰ / Ⅲ) of noninfarcted area were observed in rats after MI. Treatments were started on the 3rd day after MI and continued for another 28 days. Results Enalapril reduced LVEDP, V (m) n and collagen content as well as collagen Ⅰ / Ⅲ compared with the untreated MI group (P <0.05), and all of these effects of enalapril was partly blunted by concomitant treatment with hoe- 140 (P < However, three treatment groups had no significant differences in + dp / dtmax and had similar reductions in MAP compared with untreated MI group. Conclusions BK can improve cardiac function and prevent left Ventricular hypertrophy with myocardial fibrosis independent of blood pressure. The mechanisms of ACEI are both blockade of AngⅡ formation and inhibition of BK degradation.