Introduction: Trypanosoma cruzi infection is a serious public health problem in Latin America. Despite positive results from programs directed to the interruption of vectorial transmission, there are still millions of people infected, and a large number, at the risk of infection. Chagas disease is typically associated with cardiac complications, and chronic symptoms include heart failure and megaesophagus development. Objective: In this study, we aimed to evaluate the importance of the cardiorenal axis and renin-angiotensin-aldosterone system (RAAS) activation in experimental T.cruzi infection. We also evaluated the influence of aldosterone and the angiotensin II receptor type 1 (AT1R) on the mortality of infected mice. Methods: BALB/c mice infected with the Y strain of T.cruzi were treated with spironolactone or losartan. We assessed parasitemia, mortality, and renal and cardiac function by using non-invasive methods. Results: Our data show that AT1R promotes an important (and necessary) inotropic positive effect in the heart and minimizes acute kidney injury. Conversely, aldosterone increases the release of K+ and aggravates heart failure. It also has associated effects on the renal, cardiovascular, and cardiac electrical conduction systems. Consequently, the aldosterone antagonist reduced the mortality rate by 50%, whereas the AT1R antagonist increased it by 20%. Conclusions: The RAAS connects the cardiorenal systems, and its components differentially affect the mortality of animals experimentally infected by T.cruzi.