心肌局部血管紧张素Ⅱ激活MAPK参与运动性心肌肥大  

Angiotensin Ⅱ Activated Exercise Myocardium Hypotrophy Mediated by Mitogen- activated Protein Kinase

作　　者：侯香玉[1,2] 李维根[1,2] 张宝慧[1,2] 高云秋[1,2] 庞永正[1,2] 唐朝枢[1,2] 

机构地区：[1]北京医科大学运动医学研究所 [2]北京医科大学心血管基础医学研究所

出　　处：《中国运动医学杂志》1997年第4期257-258,279,共3页Chinese Journal of Sports Medicine

基　　金：国家自然科学基金

摘　　要：在长期游泳训练的大鼠心肌组织中，观察了ＡＲⅡ（心肌局部血管紧张素Ⅱ）的促细胞肥大效应与ＭＡＰＫ（丝裂素活化蛋白激酶）活性的关系，以探讨ＡＴⅡ促进运动心肌肥大的信息传递机制。结果表明：运动组心系数增加了２３．８％，心肌局部ＡＴⅡ和ＭＡＰＫ活性分别增加了４８．７６％和４４５．４％，二者显著相关，相关系数ｒ＝０．７８７，提示心肌局部ＡＴⅡ通过激活ＭＡＰＫ参与运动性心肌肥大的发生。The change of angiotensin Ⅱconsentration and MAPK activity in myocardium were observed to approach the pathway of angiotensin Ⅱ activated exercise myocardial hypertrophy. The resultsshowed that cardiac coefficent increased 23.8% (P<0.05) compared with control, and angiotensin Ⅱ consentration and MAPK activity in exercise group increased 48. 76% ( P < 0.01 ) and 445 . 4% (P<0.001), respectively, and r=0.787(P<0.01) between angiotensin and MAPK. Thesesuggested that angiotensin Ⅱactivated exercise myocardium hypertrophy was mediated by mitogen - activated protein kinase .

关 键 词：丝裂素 蛋白激酶 血管紧张素Ⅱ 心肌肥大 运动性 

分 类 号：R874[医药卫生—运动医学]