However, despite the partially compensated blood pressure and the absence of cardiac hypertrophy and fibrosis, we found significantly higher levels of miR-132 and miR-212 in heart (1.7- and 2.0-fold), aorta (3.5- and 2.5-fold) and kidney (1.5- and 1.8-fold) of the ET-1 treated animals as compared to controls (Figure 4C). This evidence concerns the gene EDN1 and cardiac hypertrophy.