Introduction: Aute increase in intracranial pressure (ICP) may result from cerebral hemorrhage, brain trauma, oedema or acute hydrocephalus and leads to compression of brain structures and decreased cerebral blood flow [1]. The diminished cerebral perfusion is compensated for by Cushing reflex which maintains cerebral blood flow under conditions of high ICP via elevation of blood pressure (BP) [2]. Robust evidence shows that brain angiotensin type 1 receptors (AT1Rs) play an important role in pressor response to physiological and pathological stimuli [3]. Aim: Thus, we seeked to find out how AT1Rs participate in the hemodynamic response to acutely increased ICP. Methods: Male Sprague-Dawley rats, 14-18 weeks of age, were implanted with arterial catheter for recording of blood pressure (BP) followed by implantation of two steel cannulae in the lateral cerebral ventricles (LCV). The cannula placed in the right LCV was used for intrabrain infusion for increasing ICP and for recording of ICP, while the one in the left LCV was used for administration of investigated substances. The animals were divided into 2 groups: control group LCV infused with 0.9% NaCl (n=6); and experimental group LCV infused with losartan, AT1Rs antagonist (n=6). After recording baseline BP and ICP, saline (10 µL/30sec) or losartan (10 µg/10µl/30 sec) was infused into LCV. After 5 min ICP was gradually increased by intracerebroventricular infusion of 0.9% NaCl by syringe pump at the rate of 60 µl/min till obtaining ICP of ca. 100 mm Hg. All procedures and measurements were performed under urethane (1.5g/kg b.w.) anaesthesia. Results: The pre-treatment BP and ICP were similar in control and losartan animals (95 +/- 7 mmHg, 5.8 +/- 2.8 mmHg; 97 +/- 8 mmHg, 7 +/- 1.4 mmHg, respectively). LCV administration of losartan had no effect on BP and ICP. Intrabrain infusion of saline (60 µl/min) resulted in similar increase in ICP in the control group (98 +/- 2 mmHg) and in the losartan one (99 +/- 2). In the control group increase in ICP resulted in significant elevation of BP in comparison to baseline values (paired Student t-test, p<0.05), which is typical for Cushing reflex. In the experimental group, pre-treatment with losartan diminished BP increase in response to high ICP and significantly reduced blood pressure change in comparison to the control group (unpaired Student t-test, p<0.05). Conclusions: Our results indicate that brain angiotensin type 1 receptors participate in pressor Cushing reflex response to acute ICP increase. This new finding suggests that pharmacotherapy with angiotensin receptor blockers may adversely modulate BP control under conditions of acute intracranial hypertension.