The effects of labetalol (Lab), an alpha_1 and beta adrenoceptor blocking agent, and propranolol on myocardial blood flow (MBF), infarct size (IS) and left ventricular function during coronary occlusion in the rabbits were studied. After left ventricle coronary artery was ligated, the 53 rabbits were divided into 4 groups: control, propranolol 0.5mg/kg, Lab 1mg/kg and Lab 5mg/kg. After 30 min coronary occlusion, regional blood flow was determined by radioactive biological microspheres technique. After 5 hours occlusion, left ventricular pressure and its differentiation were measured and IS was estimated with NBT staining method. The results show: Lab 1mg/kg demonstrated mainly beta adrenoceptor blockade. It slowed heart rate, diminished myocardial oxygen consumption, decreased MBF except for infarct zone and reduced IS, the effects were similar to propranolol. Furthermore, it improved left ventricular function while propranolol did not. Lab 5mg/kg blocked alpha_1 and beta receptor simultanously. It decreased arterial blood pressure and heart rate, increased blood flow of myocardium and kidney relatively, diminished myocardial oxygen requrement more markedly than propranolol and reduced IS. These imply that simultanous alpha_1 and beta blockade have some advantage over beta blockade alone in the treatment of acute myocardial infarction.

AIM: To observe the effect of angiotensinⅡ subtype 2 receptor (AT_2 receptor) on the cultured rat aortic vascular smooth muscle cells. METHODS: The plasmid contained the cDNA of AT_2 receptor was transfected into cultured rat vascular smooth muscle cells. The effects of AngⅡ, Ang Ⅱ+losartan, Ang Ⅱ+PD123319 on the expression of PCNA, the NOS activity and the cell number were observed. RESULTS: The cell number and the expression of PCNA decreased after the cells were treated with losartan. When treated with PD123319, the cell number and the expression of PCNA increased, but the expression of NOS decreased. CONCLUSIONS: These data suggest that when being activated, AT_2 receptor inhibits the proliferation of vascular smooth muscle cells and antagonizes the effect of AT_1 receptor, such an effect may be related to the activation of NOS. [

Objective:To observe the affection of angiotensin Ⅱ antagonists on the cultured subtype 2 receptor of angiotensin II transfected aortic vascular smooth muscle cells of rat.Methods:After transfected the plasmid that contained the cDNA of subtype 2 receptor of angiotensin II into cultured rat vascular smooth muscle cells, the cells were divided into three groups：cells of group 1 were treated with angiotensinⅡ,cells of group 2 were treated with angiotensinⅡand losartan,cells of group 3 were treated with angiotensinⅡ and PD123319 .After experiments，the expression of PCNA, NOS and the cell number was tested, respectively.Results：After treated with Losartan，the cell number of group 2 was(4.17±0.15)×105，the OD value of PCNA was 0.202 6±0.007 6，both of which were less than that of cells of group 3；the OD value of NOS of cells was more in group 2(0.027 5±0.002 1 ) than that in group 3 (0.016 9±0.002 0) (P＜0.01).Conclusions:It suggests that when being activated,subtype 2 receptor of angiotensin Ⅱ could inhibit the proliferation of vascular smooth muscle cells and antagonist the effect of subtype 1 receptor of angiotensin Ⅱ,such an effect may be related to the activation of NOS.