| Objection: Myocardial infarction induces global change in ventricular architecture, called post-myocardial infarction left ventricular remodeling, which involves LV dilation, myocyte hypertrophy, and interstitial fibrosis, leading to a deterioration in LV function that is associated with increased rate of mortality. Rein-angiotensin system (RAS) especial angiotensin II (Angll) plays an important role in this process, so block the activation of RAS is the key to inhibit remodeling .This study investigated the correlation between AT1. AT2 receptors mRNA expression and myocardial interstitial collagen metabolism and effects of angiotensin-converting enzyme inhibitor(ACEI) . selective angiotensin II receptor blocker (ARB) on angiotensin type I(AT,). type II(AT2) receptors . collagen type I. type III mRNA expression after myocardial infarction and speculated the possible mechanism of ACEI and ARB on the ventricular remodeling.Methods: Myocardial infarction was induced in Wistar male rats by ligation of the anterior descending coronary artery. Sham-operated rats served as controls(group A). One day after the anterior descending coronary ligation ,the operated rats were randomized to 4 groups, group B(placebo. C (Cilazapril,lmg/kg/d) ,D(valsartan,30mg/kg/d) and D(combine with two drugs by half dose). After treated with 2weeks,we measured AT1. AT2. collagen type I and type III mRNA expression by RT-PCR. The heart and body weight were also studied.Results: Body weight has not significantly different among 5 groups. Compare with group A, the heart weight and the ratio heart weight to body weight in group B were significantly increased(p<0.01),there were noAbstractsignificantly differents among group A , C ,D and E. In group B, the expression of AT, receptor mKNA were significantly increased in both infarction zone and non- infarction zone compared with group A, and the expression of AT, mRNA between infarction zone and non-infarction zone were different, infarction zone was higher than non-infarction zone(p<0.01).Both in infarction zone and non-infarction zone of group C. D. E ,the expression of AT, mRNA were significantly reduced compared with group B, but still significantly higher than group A. Among group B, C, D and E, the AT2 mRNA expression both in infarction zone and non-infarction zone were strikingly increased compared with group A, and we found that the expression of AT2 mRNA in group D and E also higher than group B. In both infarction zone and non-infarction zone, the collagen type I mRNA expression of group B was strikingly increased compared with group A and the expression of collagen type I in infarction was higher than non-infarction. In infarction zone , the collagen type I mRNA expression of group C,D,E were significantly reduced compared with group B, but still strikingly higher than group A. In non-infarction zone, the expression of collagen type I of group C. D and E were lower than group B ,and no significantly difference among group A. C. D and E. The changes of collagen type III mRNA expression were the same as collagen type I. In both infarction zone and non-infarction zone, the expression of AT1 receptor mRNA correlated with the expression of collagen type I and III.Conclusion: The expression of collagen type I and type HI mRNA were increased in myocardial tissue after infarction. Both AT, and AT2 receptor mRNA expression were strikingly increased, and angiotensin II regulated ventricular remodeling process by AT1 and AT2 receptors .Both ACEI and ARBAbstractcan reduced the expression of collagen type I and type III mRNA, but different between AT1 and AT2 mRNA expression, and increasing AT2/AT, was probably one mechanism of ACEI and ARB inhibiting ventricular remodeling after myocardial infarction.
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