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The activation of angiotensin II type 2 receptor (AT2 R) has been considered cardioprotective. However, there are controversial findings regarding the role of overexpressing AT2 R in the heart. Using transgenic mice with different levels of AT2 R gene overexpression in the heart (1, 4, or 9 copies of the AT2 R transgene: Tg1 , Tg4 , or Tg9 ), we studied the effect of AT2 R overexpression on left ventricular remodeling and dysfunction post–myocardial infarction (MI). Tg1 , Tg4 , Tg9 , and their wild-type littermates were divided into (1) sham MI, (2) MI plus vehicle, and (3) MI plus AT2 R antagonist. Treatments were started 4 weeks after MI and continued for 8 weeks. AT2 R protein and mRNA expression in the heart was significantly increased in transgenic mice, and the increase positively correlated with copies of the transgene. AT1 R protein and mRNA expression remained unchanged in Tg1 and Tg4 but slightly increased in Tg9 mice. Systolic blood pressure and cardiac phenotypes did not differ among strains under basal conditions. MI caused myocardial hypertrophy, interstitial fibrosis, ventricular dilatation, and dysfunction associated with increased protein expression of Nox2 and transforming growth factor β1 . These pathological responses were diminished in Tg1 and Tg4 mice. Moreover, the protective effects of AT2 R were abolished by AT2 R antagonist and also absent in Tg9 mice. We thus conclude that whether overexpression of AT2 R is beneficial or detrimental to the heart is largely dependent on expression levels and possibly via regulations of Nox2 and transforming growth factor β1 signaling pathways.

Effects of Cardiac Overexpression of the Angiotensin II Type 2 Receptor on Remodeling and Dysfunction in Mice Post–Myocardial Infarction