With respect to contractile performance, since systolic function was normalized in the OBL group, it is acceptable that AT1R blockade attenuated the myocardial inotropic effect derived from the endocrine role of adipose tissue, with a consequent reduction in myofibril and sarcomere recruitment; actually, ventricular hypertrophy was controlled in OBL, as supported by macro and microscopic evidence. Here, AGTR1 is linked to cardiac hypertrophy.