Relation Of The Expression And Regulation Of Angiotensin Ⅱ Type 1 Receptor With Myocardial Remodeling In Rat

The long-term sequelae of cardiovascular diseases such as hypertension, myocardial infarction, valvular heart disease, and dilated cardiomyopathy are structural changes in the heart and blood vessels that contribute to the complications of these disorders. The structural changes are mediated by the process of remodeling. Remodeling involves alterations in cellular and extracellular elements including cell migration, growth, apoptosis, and matrix modulation.Cardiovascular remodeling is initially an adaptive process to the alterations in hemodynamic or circulating forces. However, physiological remodeling can contribute to the pathophysiology of the primary disorder and may result in pathological remodeling. Cardiovascular damage occurs as pathological remodeling develops. Atherosclerosis and ventricular dilatation are examples of this phenomenon. Physiological and pathological remodeling processes are a continuum. Therefore, early blockade of remodeling can make contribution to preventing of cardiovascular complications. A myriads of data have demonstrated that remodeling is activated by mechanical or humoral factors, which are usually mediated by growth factors and vasoactive substances. In these causes, angiotensin II (Ang II) has been thought to act as a crucial stimulus for hypertrophy of cardiac myocytes and hyperplasia of cardiac fibroblasts (cardiac remodeling). So far, almost all the effects of Ang II are still thought to be mediated via type I Ang II receptor, therefore, to elicit if the mRNA level of AT₁ is correlated with the mRNA levels of sarcoplasmic reticulum Ca²⁺ — ATPase gene (SERCA2a), collagen I and III genes (the expression change of the latter...