Objective To compare protective effects of chronic brain natriuretic peptide (BNP) infusion and enalapril administration on post myocardial infarction (MI) ventricular remodeling, and to investigate their effects on the matrix metalloproteinase (MMPs) expression in myocardium. Methods Rats were randomly assigned to sham-operated group, MI group in which MI models were prepared by coronary ligation, BNP group in which MI rats received chronic BNP infusion [0.06mg/(kg?min)] and enalapril group in which MI rats received enalapril administration [10mg/(kg?d)]. Ventricular remodeling and heart function were estimated by echocardiography (ECG), immunohistochemistry, ELISA and Western blot. Results Exogenous BNP infusion maintained a higher BNP level in heart tissue. BNP treatment achieved similar protective effects as enalapril therapy on postinfarction myocardial remodeling. Both BNP and enalapril inhibited the increase of left ventricular weight index by 13.2% and 16.9% respectively, (P＜0.05), decreased left ventricle end pressure by 33.0% and 45.8% respectively(P?0.05). ECG results demonstrated that left ventricular end-diastolic diameter (LVEDD) and fractional shortening (FS) were more satisfactory in BNP and enalapril groups than in MI group [LVEDD: (8.8±0.6) mm in MI group, (7.5±0.7) mm in enalapril group, and (7.5±1.0) mm in BNP group, P＜0.05; FS: (19.2±2.6)% in MI group, (27.7±5.6)% in enalapril group, and (27.5±3.9) % in BNP group, P＜0.05]. Both enalapril and BNP inhibited collagen deposition in non-infarcted area obviously, especially typeⅠ collegen, by (6.8?1.4)% in MI group, (4.0?0.9)% in enalapril group, and (3.7±1.1)% in BNP group respectively(P＜0.05). BNP infusion increased cyclic guanosine monophosphate (cGMP) concentration in cardiac tissue more significantly than enalapril, while inhibited angiotensin Ⅱ less significantly than enalapril. BNP infusion did not lead to obvious change of MMP-2 and MMP-9 content in non-infarcted area. Conclusion Continuous BNP infusion may play cardiac protection roles through cGMP mediated signal pathway, including inhibiting postinfarction cardiac hypertrophy, LV enlargement and collagen deposition, so as to improve heart function, while it exerts no influence on MMP-2 and MMP-9 content in non-infarcted area.