芦沙坦和苯那普利对心肌丝裂素活化蛋白激酶的抑制作用  

INHIBITING EFFECTS OF BENAZEPRIL AND LOSARTAN ON MYOCARDIAL MITOGENIC ACTIVATED PROTEIN KINASE

作　　者：张丽萍[1] 郑秋甫[1] 何昆仑[1] 唐朝枢[1] 曾强[1] 范英鲜[1] 

机构地区：[1]解放军总医院,北京100853

出　　处：《解放军医学杂志》2001年第7期527-528,共2页Medical Journal of Chinese People's Liberation Army

摘　　要：为探讨芦沙坦和苯那普利对心肌丝裂素活化蛋白激酶的抑制作用 ,以Wistar Kyoto (WKY)大鼠作为对照 ,老龄前期自发性高血压大鼠 (SHR)随机分为对照组、苯那普利 [10mg/ (kg·d) ]及芦沙坦 [30mg/ (kg·d) ]治疗组 ,治疗期为 3个月。结果发现 ,SHR对照组血压、心肌肥厚指标 (心脏重 /体重、左室 +室间隔 /体重 )、血中及心肌中血管紧张素Ⅱ (AⅡ )及丝裂素活化蛋白激酶 (MAPK)明显高于WKY大鼠对照组 ,经苯那普利及芦沙坦治疗后 ,除芦沙坦组血中及心肌中AⅡ无下降外 ,上述指标均显著降低 (P <0 .0 1)。说明AⅡ及MAPK参与了SHR的血压升高及心肌肥厚的形成 ;苯那普利及芦沙坦可抑制AⅡ及MAPK的活性 。SHRs were randomly divided into three groups: SHRs control group, Benazepril group (10mg/kg·d) and Losartan group (30mg/kg·d). WKYrats act as the normal control group. The animals were treated for 3 months. Compared with WKY rats, the blood pressure, angiotensinⅡ(AⅡ)levels in blood and myocardium, mitogen activated protein kinase (MAPK) activity, and myocardial hypertrophy in SHRs control group were increased ( P <0.01).A significant decrease in blood pressure, MAPK activity, and marked regression of myocardial hypertrophy were observed in Benazepril group. In losartan group ,we found the same results, except that AⅡlevel in plasma and cardiac tissue were still at high levels.These results suggest AⅡand MAPK may mediate cardiac hypertrophy in SHR. Benazepril and Losartan can inhibit action of AⅡand MAPK so that they can lower blood pressure and regress cardiac hypertrophy.

关 键 词：有丝分裂素激活蛋白激酶类 血管紧张素Ⅱ 芦沙坦 苯那普利 心肌肥厚 

分 类 号：R542.2[医药卫生—心血管疾病]