The relevance of cell volume and mechanical stretch as a regulators of chloride or potassium channels and the role of AT1 receptors as mechanosensors independently of Ang II indicates that during myocardial ischemia or heart failure, abnormalities on the electrical properties of the heart and cardiac remodeling can be produced independently of the RAS but able to alter the effect of Ang II and Ang (1–7). This evidence concerns the gene AGT and heart failure.