ACTIVATION OF ANGIOTENSIN-CONVERTING ENZYME EXPRESSION IN INFARCT ZONE FOLLOWING MYOCARDIAL-INFARCTION

被引:74
作者
PASSIER, RCJJ
SMITS, JFM
VERLUYTEN, MJA
STUDER, R
DREXLER, H
DAEMEN, MJAP
机构
[1] UNIV LIMBURG, DEPT PATHOL, CARDIOVASC RES INST MAASTRICHT, 6200 MD MAASTRICHT, NETHERLANDS
[2] UNIV FREIBURG, DEPT MOLEC CARDIOL, D-79106 FREIBURG, GERMANY
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 1995年 / 269卷 / 04期
关键词
MESSENGER-RNA; LOCALIZATION; RAT HEART; COMPETITIVE REVERSE TRANSCRIPTASE-POLYMERASE CHAIN REACTION;
D O I
10.1152/ajpheart.1995.269.4.H1268
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
In the present study we quantified angiotensin-converting enzyme (ACE) mRNA and localized ACE mRNA and protein in the infarcted rat heart. Wistar rats underwent ligation of the left descending coronary artery, resulting in myocardial infarction (MI) or a sham operation. At different times (1-90 days) after surgery (n = 3 each), the heart was removed and divided into the right ventricle (RV), septum (Se) and left ventricle (LV). ACE mRNA was quantified by competitive reverse transcriptase-polymerase chain reaction (RT-PCR). At 4 and 7 days after MI, we found a 2.8-fold increase of ACE mRNA (n = 3; P less than or equal to 0.05) in the infarcted LV compared with the LV of the sham group. No increases of ACE mRNA were found in the noninfarcted hypertrophied compartments. ACE activity increased 2.6- and 3.6-fold in the infarcted LV at 7 and 90 days after MI, respectively. In situ hybridization and immunohistochemistry showed increased ACE mRNA and protein density in the border zone of the infarcted area, predominantly in the endothelial cells lining capillaries. In the noninfarcted myocardium ACE mRNA and protein were confined to endothelial cells of the larger vessels. From these data we conclude that the intracardiac RAS is involved in the healing of the scar after MI in the rat, possibly giving rise to neovascularization. Furthermore, the data suggest that the intracardiac ACE is not necessarily associated with hypertrophy in the rat heart after MI.
引用
收藏
页码:H1268 / H1276
页数:9
相关论文
共 48 条
[1]  
ANVERSA P, 1984, AM J PATHOL, V116, P504
[2]   RENIN-ANGIOTENSIN SYSTEM INVOLVEMENT IN PRESSURE-OVERLOAD CARDIAC-HYPERTROPHY IN RATS [J].
BAKER, KM ;
CHERNIN, MI ;
WIXSON, SK ;
ACETO, JF .
AMERICAN JOURNAL OF PHYSIOLOGY, 1990, 259 (02) :H324-H332
[3]   ANGIOTENSIN-II STIMULATION OF PROTEIN-SYNTHESIS AND CELL-GROWTH IN CHICK HEART-CELLS [J].
BAKER, KM ;
ACETO, JF .
AMERICAN JOURNAL OF PHYSIOLOGY, 1990, 259 (02) :H610-H618
[4]   ANGIOTENSIN-II-STIMULATED PROTEIN-SYNTHESIS IN CULTURED VASCULAR SMOOTH-MUSCLE CELLS [J].
BERK, BC ;
VEKSHTEIN, V ;
GORDON, HM ;
TSUDA, T .
HYPERTENSION, 1989, 13 (04) :305-314
[5]  
BRILLA CG, 1993, EUR HEART J, V14, P57
[6]   COLLAGEN-METABOLISM IN CULTURED ADULT-RAT CARDIAC FIBROBLASTS - RESPONSE TO ANGIOTENSIN-II AND ALDOSTERONE [J].
BRILLA, CG ;
ZHOU, GP ;
MATSUBARA, L ;
WEBER, KT .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1994, 26 (07) :809-820
[7]  
CLEUJENS JPM, IN PRESS AM J PATHOL
[8]   ANGIOTENSIN-II INDUCES SMOOTH-MUSCLE CELL-PROLIFERATION IN THE NORMAL AND INJURED RAT ARTERIAL-WALL [J].
DAEMEN, MJAP ;
LOMBARDI, DM ;
BOSMAN, FT ;
SCHWARTZ, SM .
CIRCULATION RESEARCH, 1991, 68 (02) :450-456
[9]  
DANILOV SM, 1993, J HYPERTENS, V11, pS232
[10]   DETECTION OF ANGIOTENSIN-I AND ANGIOTENSIN-II IN CULTURED RAT CARDIAC MYOCYTES AND FIBROBLASTS [J].
DOSTAL, DE ;
ROTHBLUM, KN ;
CONRAD, KM ;
COOPER, GR ;
BAKER, KM .
AMERICAN JOURNAL OF PHYSIOLOGY, 1992, 263 (04) :C851-C863