On the other hand, as vascular reactive oxygen species (ROS) production can be induced by ET-1 and Ang II [28, 29], we chose to investigate the role of the renin-angiotensin and endothelin system in the hypotensive response of the EESM because it is known that the direct inhibition of the action of ET-1 can prevent the effects of Ang II from stimulating cardiac hypertrophy [28]. The gene discussed is EDN1; the disease is cardiac hypertrophy.