Intro: Stroke, a cerebrovascular disease, is the second leading cause of death in the world. Patients who survive stroke present physiological alterations and prognostic depends on the affected area. In this regard, stroke in the insular cortex (IC) results in marked sympathetic-mediated increase in baseline heart rate, cardiac molecular changes and arrythmias. Therefore, investigating strategies that can alleviate post-insular stroke consequences becomes extremely relevant. We have recently described an experimental model of right side insular hemorrhagic stroke in rats that reproduces some physiological alterations observed in humans, including marked increases in cardiac sympathetic output (Marins FR et al. 2020, 2021). Evidence indicates that the renin-angiotensin system (RAS) peptides interact with the sympathetic nervous system (Fontes MAP et al., 2016). Aims: Here, we evaluated the effect of angiotensin II (Ang II) AT₁ receptor blocker, losartan, on cardiovascular changes generated from experimental hemorrhagic stroke at the IC of rats. Methods: Experiments were conducted in accordance with the U.S. NIH Guide for the Care and Use of Laboratory Animals and approved by CEUA UFMG; protocol 112/2019). Wistar rats were: 1) anesthetized (ketamine 80mg/kg – xylazine 7 mg/kg); 2) submitted to unilateral nanoinjection of blood into the IC (Stroke IC; 200 nL; n=6) or saline into the IC (Sal IC; NaCl 0.9%, 200 nL; n=6; control), and 3) prepared for recording of mean arterial pressure (MAP) and heart rate (HR). Just after experimental stroke, separated groups of rats were submitted to three days of treatment (single daily intraperitoneal dose) of losartan (Los i.p.; 10 mg/kg) or saline (Sal i.p.; NaCl 0.9%, 0.1ml /100g). Results: Stroke IC rats showed elevated baseline HR when compared with the Sal IC group (422 ± 10 bpm vs 365 ± 6 P<0.01). Baseline MAP was similar between groups. In Stroke IC rats, treatment with Los i.p. restored HR to baseline levels and decreased baseline blood pressure values when compared with Stroke IC rats treated with Sal i.p. (HR: Los i.p. 358 ± 7 vs Sal i.p. 428 ± 10 bpm P<0.01; MAP: Los i.p. 99 ± 2 vs Sal i.p. 111 ± 2 mmHg P<0.01). The effects produced by Los in Stroke IC rats were prevented by concomitant treatment with Ang-(1-7) antagonist, A-779 (200 µg/kg SC). In agreement with this observation losartan treatment also increased the cardiac expression of Ang-(1-7)/Mas, receptor (0.93 a.u. Sal i.p. vs 1.6 a.u. Los i.p. P=0.03). Conclusions: The present data suggests that AT₁ receptors blockade may reduce the impact of cardiac sympathetic activity exacerbation observed after insular stroke as well as promote a protective reduction in baseline blood pressure values. At least part of these effects may involve activation of Ang-(1-7)/Mas receptors. The present study indicates that immediate treatment with losartan may help to minimize cardiovascular risk in the acute phase after insular stroke. Support: FAPEMIG APQ-01128-21; CNPq.