Myocardial remodeling implies an alteration in the extracellular matrix composition and distribution. Accordingly, we found in our array analysis the upregulation of collagen type I and IV in immunized rat hearts. Collagen I and III maintain the tissue structure, transmit forces throughout the myocardium and contribute to the elastic properties of the myocardium. The increased accumulation of collagen I and III has been associated mostly with fibrosis. Type IV and VI collagens are components of the basal lamina and favors cell adhesion. The increased expression could be involved in the alteration of extracellular matrix cell interaction. In human dilated cardiomyopathy, collagen is degraded by metalloproteinases and is replaced by fibrous intercellular deposits. Zhou et al found increased MMP2 expression and activity in their a1D-AR-AB immunization study. We did not observe any increased metalloproteinase or tissue inhibitors of metalloproteinases. Other up-regulated genes encode molecular regulators of energy metabolism. The peroxisome proliferator-activated receptor gamma coactivator 1-alpha activates multiple genes that are responsible for fatty acid uptake and oxidation and for oxidative phosphorylation. The development of heart failure is accelerated by Ppargc1a deficiency, suggesting that this coactivator may have a cardioprotective function. Another important observation is the fact that genes coding for important Ca2+ regulating proteins, such as ATPase, Ca2+ transporting, slow-twitch coding for the sarcoplasmic/ endoplasmic reticulum calcium ATPase, the cardiac ryanodine receptor 2, and the L-type calcium channel, alpha 1 C subunit were all up-regulated. The overexpression of SERCA2a in Heparin sodium diseased hearts has been shown to result in the recovery of contractility and in improved survival, corresponding with an improvement in energy consumption. Furthermore, SERCA overexpression decreases or prevents cardiac hypertrophy. In our earlier study we found that acute administration of purified a1-AR-autoantibodies from patients or rabbit a1A-AR-AB to neonatal cardiomyocytes affected Flunarizine 2HCl intracellular Ca2+ at two different levels, namely the acute, shortterm elevation of intracellular Ca2+, and the increased transcript expression of Cacna1c.