心肌血管紧张素Ⅱ在运动和高血压性心肌肥大时肌球蛋白重链变化中的作用

运动和高血压心肌肥大的细胞表型改变明显不同，心肌局部血管紧张素Ⅱ（ＡｎｇⅡ）参与运动和高血压心肌肥大形成。为了解心肌局部ＡｎｇⅡ是否参与两种不同心肌肥大细胞表型变化调节，本实验对正常和自发性高血压大鼠（ＳＨＲ）运动后心肌ＡｎｇⅡ与肌球蛋白重链（ＭＨＣ）异型变化进行相关分析，结果表明正常安静大鼠心肌ＡｎｇⅡ与ａ－和β－ＭＨＣ变化无明显相关性（ｒ＝０．１７４７：０．１７３２，Ｐ＞０．０５），但经过１２周游泳训练运动后，心肌ａ－ＭＨＣ增加，ＡｎｇⅡ含量升高，两者呈正相关（ｒ＝０．７７２３，Ｐ＜０．０５）。ＳＨＲ心肌ＡｎｇⅡ和β－ＭＨＣ比ＷＫＹ高８８．０２％和４６．８９％，两者呈正相关（ｒ＝０．８７０５，Ｐ＜０．０５），ＳＨＲ心肌ＡｎｇⅡ与ａ－ＭＨＣ呈负相关（ｒ＝－０．８６２２，Ｐ＜０．０５），ＷＫＹ心肌ＡｎｇⅡ与ａ－和β－ＭＨＣ之间无明显相关性（ｒ＝０．２９３５；０．０２６３，Ｐ＞０．０５）。ＳＨＲ经１０周游泳运动后，心肌ＡｎｇⅡ含量下降，β－ＭＨＣ向ａ－ＭＨＣ逆转，ＡｎｇⅡ与ａ－／β－ＭＨＣ呈正相关（ｒ＝０．７９３４：Ｐ＜０．０５）。以上结果提示心肌局部ＡｎｇⅡ在运动性心肌肥大中可能具有对ａ－ＭＨＣ表达上调作用?

Correlation of Angiotensin Ⅱ in Myosin Heavy Chain Expression of Myocardium in Exercise-Induced and Hypertensive Cardiac Hypertrophy

Some evidences suggested that angiotensin Ⅱ ( Ang Ⅱ ) in myocardium may play an important role as s di- rect growth factor in exercise - induced and hypertensive cardiac hypertrophy.But expression of myosin heavy chain( MHC) isoenzymes was shifted to β- MHC from α-MHC isoenzyme in hypertensive cardiac hypertrophy and to -MHC from β-MHG isoenzyme in exercise-induced cardiac hypertrophy.The cause of this change is unknown . To understand the role of Ang Ⅱin this phenomenon , the correlation of Ang Ⅱ concentration in myocardium with the expressin of MHC isoenzymes in models of exercise-induced and hypertensive cardiachypertrophy was studied.The rats were divided into 5 groups ;Wistar-Kyoto (WKY),spontaneously Hyperten- sive Rats( SHR) , SHR with swimming for 10 weeks(SHR-SWI),S.D,control (SD)and S.D.swimming for 12 weeks(SD-SWI).The results showed that the level of Ang /Ⅱ in myocardium correlated positively with thedegree of cardiac hypertrophy among SHR,SHR-SWI and SD-SWI(P<0.05).But level of Ang Ⅱ corre-lated positively with αMHC/β-MHC isoenzyme ratio in SD-SWI(p<0.05)and negatively with α-MHC/ β-MHC isoenzyme ratio in SHR(P<0.05) In addition ,we found that level of Ang Ⅱ correlated positively with α- MHCβ - MHC isoenzyme ratio in SHR-SWI(P<0.05).Thus our data suggested that the increase in α- MHC/β- MHC isoenzyme ratio expression could be mediated via Ang Ⅱ in myocardium by exercise.