A possible explanation for this was given recently by our group, demonstrating that this effect was AT1R-dependent and partially AT2R-dependent: while in the absence of blockade of angiotensin II receptors the myocardium presents a progressive decrease in contractility during ischemia, the blockade of AT1R is able to prevent this deterioration after stretch (Neves et al., 2013). This evidence concerns the gene AGTR1 and ischemia.