Cardiac RAS is involved in paracrine/autocrine regulation of cardiac function, where it primarily controls cell growth and proliferation, but also activates different signaling pathways within cardiovascular cells. Locally produced angiotensin II (Ang II) induces fibrosis and heart hypertrophy via activation of Ang II AT1 receptor, while activation of Ang II AT2 receptor has opposite effects. Previous studies were performed on males only. Our findings suggest that FRD induces gender specific changes in the expression of RAS components in the heart. In the heart of male rats 10% FRD decreased Ang II AT2 receptor protein level, while it totally abolished mRNA synthesis of Ang II AT2 receptor. E2 replacement therapy reversed the effects of FRD on RAS component expression, which is reflected as decreases in ACE and Ang II AT1 receptor levels and increases of ACE2 and Ang II AT2 receptor levels. In the heart of ovariectomized rats 10% FRD activating NFκB, where E2 showed beneficial effects by inhibiting it. Proinflammatory effect of high fructose diet and anti-inflammatory action of E2 detected in the heart of ovariectomized rats could be connected with the changes observed in cardiac insulin signaling through Akt pathway.We can conclude that FRD affects cardiac renin angiotensin system by stimulating harmful RAS axis - ACE/ Ang II AT1 receptor, and by inhibiting protective molecules - ACE2 and Ang II AT2 receptor. Estradiol showed beneficial effects by causing a reverse of those changes.