The Correlation Of Pulmonary Hypertension And Ang(1-7)、AngⅡ、ACE2

Objective : To build the rat model of pulmonary hypertension with monocrotaline-induced,and discuss the correlationt of pulmonary artery pressure and angiotensin1-7(Ang1-7),angiotensin Ⅱ(Ang Ⅱ),angiotensin-coverting enzyme(ACE2).Methods:Tirty male SD rats were randomly divided into three groups with ten each group : control group(A group),pulmonary hypertension group(B group),diltiazem group(C group).The rats in B,C group were injected with 50mg/kg of MCT subcutaneously,and the rats in A group were injected with equal saline. Since the next day after MCT injected,,diltiazem(25mg/kg/d) was administered by gavage to rats inin C group,respectively;and distilled water was given by gavage to rats in A group and B group.Three weeks after MCT injected,mean pulmonary artery pressure(m PAP)and right ventricular systolic pressure(RVSP)was measured by right heart catheterizationthe.The concentration of Ang1-7,Ang Ⅱ were detected by Enzyme-linked immunosorbent assay(ELISA); Hematoxylin-eosin(HE) staining were observed for the morphological changes of lung tissure;Immunohistochemistry were observed for the change of ACE2 expression in lung tissure.Result:The mean pulmonary artery pressure(m PAP),right ventricular systolic pressure(RVSP), and Ang1-7,Ang Ⅱ in B group were significantly increased than that in A group(P<0.001),C group were decreased significantly than that in B group(P<0.001),but decreased than that in A group(P<0.001).The changes of lung tissure in B group were inflammatory cell infiltration 、 the middle-level of pulmonary artery is thicking obviously,luminal stenosis,pulmonary artery intimal hyperplasia as compared with A group, and that changes in C group were between A and B group.The expression of ACE2 on lung tissure in B group were decreased as well compared with A group(P<0.05), and that changes in C group were between A and B group(P<0.05)..Conclusion: Ang1-7,Ang Ⅱ,ACE2 were significantly changed in pulmonary hypertension,this shows that the imbalance of the rennin-angiotensin system closely associated with pulmonary hypertension.