Loss of myocardium due to acute myocardial infarction may cause acute heart failure and future left ventricular dysfunction. During heart failure, homeostatic mechanism will be activated and the renin-angiotensin system may play a role in congestive heart failure. Its primary components are angiotensinogen, renin, angiotensin converting enzyme, and angiotensin.

According to the recent improvement of molecular biologic technique, it is possible to know the angiotensinogen nucleotidde sequence, amino acid sequence, and tertiary structure and to detect very small amount of material from tissue.

The aim of the present study was to examine the change of expression of the liver angiotensinogen mRNA, a component of the circulation renin-angiotensin system in rats after myocardial infarction.

Female Sprague-Dawley rats(body weight 200-250g) were anesthetized and subjected either to left coronary artery occlusion or to sham operation. And the rats were sacrificed at 1 hours, 4 hours, 18 hours, 24 hours, 3 days, 7 days, 1 week, 2 weeks and 3 weeks. Northern blot analysis was performed.

The liver angiotensinogen amRNA levels were elevated at 4 hours, 18 hours, 24 hours after myocardial infarction and reduced to control values at 3 days(max 5-fold). The liver angiotensinogen mRNA levels were lesser elevated at 4 hours, 18 hours, 24 hours after sham operation(max 1.8-fold).

The renin-angiotensin system is one of the major regulators of blood pressure and fiuid and electrolyte homeostasis. It appears that the circulating renin-angiotensin system is activated acutely after myocardial infarction and is then turned off at cardiovascular compensation.