Angiotensin Receptor Blocker Affects AT-1 And AT-2 Expression In AMI Rat

Objective: Valsartan is the antagonist of AT1 receptor which has specificity and highly selectivity, it can effectively antagonize AngII by the way of combining with AT1 receptor.In addition, local heart and blood vessel AngII can induce cardiac hypertrophy via the non-hemodynamic function of paracrine and autocrine, AngII can directly stimulate the growth of myocardial and vascular smooth muscle cells after AMI. Valsartan can increase the AngII in plasma and activate AT2R, antagonize the expension of vessel which mediate by AT1, inhibition cell proliferation. Finally, AngII can decrease the infarction area, the sedimentary of collagen and ventricular remodel by the way of endothelial productions such as NO, prostaglandin, bradykinin. IN this study, we need to observe the expression of AT1 and AT2 receptors after AMI in rats, investigate the protective mechanism of Valsartan in AMI.Methods: Divide 80 Wistar rats into 3 group, A group: control group 20, B group: model group 30(AMI group), C group: medication group 30 (drug intervention +AMI). C group were given 20mg/kg. d Valsartan to stomach 2 weeks, A group and B group were given the same dose NS. Rat M1 models: deal with drug after 2 weeks, fix the ether anesthesia rats at the operating table, expose the rat heart at 4-5 intercostal, find the LAD and ligate it, after that, put it into thoracic cavity and exclude the blood and gas of the thoracic cavity, close the thoracic cavity, the totle time was limit in 30s, A group do not ligate the coronary. After ligate the coronary, the ST section rise obviously proves AMI model is successful. Dying the specimen of myocardial, determination the pathology changes. Determination mRNA expression of AT-1R, AT-2R via RT-PCR.Results: Compare with control group, the expression of AT-1R,AT-2R in AMI notably increase. The mRNA expression of AT-2 increase in medication group, AT-2 decrease,the infarction area decrease.Conclusion: Valsartan can decrease the infarction area, reduce ventricular remodel and protect the cardiac function via improving the the mRNA expression of AT-2, decreasing the mRNA expression of AT-1.