Wistar-Kyoto rats underwent myocardial infarction (MI) or sham surgery. At different time points after surgery (1-90 days), hearts were removed and divided into infarcted left ventricle (LV), noninfarcted septum, and right ventricle. The tissues were used for total RNA isolation or Formalin fixation for in situ hybridization (ISH). Renin and angiotensinogen mRNA contents were quantified by the competitive reverse transcriptase polymerase chain reaction. We found a 4-, 14-, and 8-fold increase (P < 0.05, n = 6) in renin mRNA in the infarcted LV at 2, 4, and 7 days after MI, respectively. No differences were observed between angiotensinogen mRNA levels in sham and infarcted hearts. ISH at 4 days after surgery revealed a dense renin mRNA labeling around the infarcted area, whereas ISH of angiotensinogen displayed an overall low density in the myocardium with somewhat higher levels in the epicardium of sham and MI animals. Atrial natriuretic factor mRNA, a marker for cardiac hypertrophy, was approximately twofold higher in all compartments of the hearts after MI. The low amounts of renin and angiotensinogen mRNA in the noninfarcted hypertrophied myocardium indicate that the intracardiac synthesis of these components does not play a dominant role in the development of cardiac hypertrophy in the rat heart after MI. In addition, the increased renin mRNA expression in the border zone of the infarcted LV suggests a role for intracardiac angiotensin II in infarct healing.
Mast cells in the rat heart during normal growth and in cardiac hypertrophy.