Objectives To investigate the effects of adrenergic receptor antagonist (metoprol- ol or prazosin) on myocardial α1-AR density and the changes of ventricular effective refractory period disper- sion (VERP-D) in rabbits after myocardial infarction. Methods twenty-four adult male New Zealand rab- bits were divided into four groups at random: control group ( n = 6 ) ; MI with placebo group ( n = 6 ) ; MI with metoprolol group ( n = 6) ; MI with prazosin group ( n = 6 ). The rabbits received corresponding drugs for seven days, beginning at the first day after MI with metoprolol 5 mg · kg-1 · d-1 or prazosin 0.5 mg · kg-1 · d-1. On the seventh day after MI, VERP-D and myocardial α1-AR density were measured and meanwhile, myocardial β-AR was also measured. Results In the placebo group, the density of ventricu- lar α1-AR was increased in comparison with control group (α1-AR in normal region 36. 9 ± 0. 2 vs 27. 3 ± 0. 9 fmol mg-1 pro-1 ,P <0.01; α1-AR in ischemic region 33.0±0.9 vs 26.6±0.4 fmol mg-1 pro-1 P<0.01).In the metoprolol group, it was also increased in compari- son with control group(α1-AR in normal region 44. 7 ± 1.5 vs 27.3 ±0.9 fmol mg-1 pro-1 ,P <0. 01; α1-AR in ischemic region 33. 6 ± 0. 5 vs 26. 6 ± 0. 4 fmol mg-1 pro-1 , P <0. 01 ). Meanwhile the density of ven- tricular α1-AR in normal region in the metoprolol group was increased in comparison with placebo group (44.7 ± 1.5 vs 36. 9 ±0.2 fmol mg-1 pro-1 ,P <0. 01). While it decreased in the prazosin group in comparison withcontrol group (α1 -AR in normal region 22. 5 ± 0 . 6 vs 27.3±0.9 fmol mg-1 pro-1,P<0.01; α1-AR in ische- mic region 20.9±0.4 vs 26.6 ±0.4 fmol mg-1 pro-1 , P <0.01). VERP-D was increased after MI(P <0.01). After treatment with metoprolol or prazosin, VERP-D was decreased ( P < 0. 01 ). Conclusions After a- cute MI, α1-AR of ventricular myocardium was upregu- lated, which may be accompanied by its activitation. The density of myocardial α1-AR became upregulated more dramatically treated with metoprolol and downreg- ulated with prazosin. When treated with metoprolol or prazosin, VERP-D decreased. Objectives To investigate the effects of adrenergic receptor antagonist (metoprolol or prazosin) on myocardial α1-AR density and the changes of ventricular effective refractory period dispergis (VERP-D) in rabbits after myocardial infarction. Methods twenty-four adult male New Zealand rab-bits were divided into four groups at random: control group (n = 6); MI with placebo group (n = 6); MI with metoprolol group (n = 6); MI with prazosin group . The rabbits received corresponding drugs for seven days, beginning at the first day after MI with metoprolol 5 mg · kg -1 · d -1 or prazosin 0.5 mg · kg -1 · d -1 On the seventh day after MI, VERP -D and myocardial α1-AR density were measured and meanwhile, myocardial β-AR was also measured. Results In the placebo group, the density of ventricule-lar α1-AR was increased in comparison with control group (α1-AR in normal region 36. 9 ± 0. 2 vs 27. 3 ± 0.9 fmol mg-1 pro-1, P <0.01; α1-AR in ischemic region 33.0 ± 0.9 v s 26.6 ± 0.4 fmol mg-1 pro-1 P <0.01) .In the metoprolol group, it was also increased in compari son with control group 44 ± 1.5 vs 27.3 ± 0.9 fmol mg -1 pro-1, P <0.01; α1-AR in ischemic region 33. 6 ± 0.5 vs. 26. 6 ± 0.4 fmol mg-1 pro-1, P <0.01). Meanwhile the density of ventricular tachycardia α1-AR in normal region in the metoprolol group was increased in comparison with placebo group (44.7 ± 1.5 vs 36. 9 ± 0.2 fmol mg-1 pro-1, P <0.01). in the prazosin group in comparison with the control group (α1-AR in normal region 22. 5 ± 0.6 vs 27.3 ± 0.9 fmol mg-1 pro-1, P <0.01; α1-AR in ischemic region 20.9 ± 0.4 vs (P <0.01). After treatment with metoprolol or prazosin, VERP-D was decreased (P <0.01). Conclusions After a-cute MI, α1-AR of ventricular myocardium was upreguated, which may be accompanied by its activitation. The density of myocardial α1-AR became upregul ated more dramatically treatedwith metoprolol and downreg- ulated with prazosin. When treated with metoprolol or prazosin, VERP-D decreased.