Angiotensin type 1 receptor mediates thyroid hormone-induced cardiomyocyte hypertrophy through the Akt/GSK-3β/mTOR signaling pathway

Several studies have implicated the renin angiotensin system in the cardiac hypertrophy induced by thyroid hormone. However, whether Angiotensin type 1 receptor (AT 1 R) is critically required to the development of T 3 -induced cardiomyocyte hypertrophy as well as whether the intracellular mechanisms that are triggered by AT 1 R are able to contribute to this hypertrophy model is unknown. To address these questions, we employed a selective small interfering RNA (siRNA, 50 nM) or an AT 1 R blocker (Losartan, 1 μM) to evaluate the specific role of this receptor in primary cultures of neonatal cardiomyocytes submitted to T 3 (10 nM) treatment. The cardiomyocytes transfected with the AT 1 R siRNA presented reduced mRNA (90%, P