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

In the present study we quantified angiotensin-converting enzyme (ACE) mRNA and localized ACE mRNA and protein in the infarcted rat heart. W istar rats underwent ligation of the left descending coronary artery, resulting in myocardial infarction (MI) or a sham operation. At differ ent times (1-90 days) after surgery (n = 3 each), the heart was remove d and divided into the right ventricle (RV), septum (Se) and left vent ricle (LV). ACE mRNA was quantified by competitive reverse transcripta se-polymerase chain reaction (RT-PCR). At 4 and 7 days after MI, we fo und 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 inc reases of ACE mRNA were found in the noninfarcted hypertrophied compar tments. ACE activity increased 2.6- and 3.6-fold in the infarcted LV a t 7 and 90 days after MI, respectively. In situ hybridization and immu nohistochemistry showed increased ACE mRNA and protein density in the border zone of the infarcted area, predominantly in the endothelial ce lls lining capillaries. In the noninfarcted myocardium ACE mRNA and pr otein were confined to endothelial cells of the larger vessels. From t hese data we conclude that the intracardiac RAS is involved in the hea ling of the scar after MI in the rat, possibly giving rise to neovascu larization. Furthermore, the data suggest that the intracardiac ACE is not necessarily associated with hypertrophy in the rat heart after MI .