In addition, left ventricular myocyte hypertrophy was observed and Zomepirac sodium salt olmesartan significantly inhibited it, which was associated with the prevention of HF and ventricular arrhythmia induction in Vitamin E Gaq-TG mice. Moreover, mRNA expression of ANF, b-MHC, and BNP was significantly upregulated in Gaq-TG hearts compared with that in NTG mouse hearts and decreased by olmesartan in Gaq-TG hearts. These results suggest that transient Gaq activation causes activation of the local renin-angiotensin system, leading to progressive heart failure and ventricular arrhythmias in Gaq-TG mice. These findings suggest that the cardiac renin-angiotensin system plays an important role in the development of cardiac hypertrophy and heart failure, even if the initiating stimulus of cardiac Gaq activation does not result from angiotensin II type I receptor stimulation. Several studies have demonstrated that cardiac remodeling is associated with increases in AT1 receptor protein expression. Moreover, olmesartan suppressed cardiac AT1 receptor levels in hypertensive rats. In this study, the protein expression levels of AT1 receptor were not changed in Gaq-TG hearts compared with those in NTG hearts. Moreover, olmesartan significantly increased the expression of AT1 receptor in Gaq-TG mouse hearts. The reason for the discrepancy between the previous and present results is uncertain. In fact, cardiac dysfunction is severe in this Gaq-TG mouse compared with that in animals used in previous studies. Moreover, the duration of olmesartan treatment was much longer in this study than in the previous study. Those differences may explain the discrepancy. In any case, our present results suggest that AT1 receptor activation plays important roles in the development of heart failure and ventricular arrhythmias in this model. It is known that myocardial ACE is a possible substrate for cardiac fibrosis. In this study, the protein expression of ACE was increased significantly in Gaq TG mouse hearts compared with that in NTG mouse hearts.Moreover, the left ventricular fibrosis and mRNA expression of CTGF and collagen type I were also significantly increased in Gaq-TG mouse hearts. Olmesartan decreased the increased left ventricular fibrosis and the mRNA expression of CTGF and collagen type I, suggesting that the reninangiotensin system participates in the development of cardiac fibrosis in this model.