Introduction: Increasing evidence points to the key role of neurogenic component in cardiovascular diseases (1). High load of salt in diet contributes to the development of essential hypertension. One of the possible mechanisms linking salt intake with hypertension is an increased concentration of sodium ions in the cerebrospinal fluid (CSF), which rearranges central control of the cardiovascular system (2). Renin-angiotensin-aldosterone system is a key regulator of sodium balance and plays a culprit role in triggering and maintaining elevated arterial pressure (3). In the present study we aimed at finding out if increased CSF sodium ions alter the control of circulatory system and whether it may be mediated by brain angiotensin type 1 receptors (AT1Rs) for angiotenin II in normotensive rats. Methods: The study was performed on adult Sprague-Dawley male rats. The animals were implanted with L-shaped cannulae connected to osmotic mini-pumps for 2-week intracerebroventricular (ICV) infusions of either isoosmotic saline (0.9% NaCl, 5 μl/hr), hyperosmotic saline (5% NaCl, 5 μl/hr) or AT1Rs blocker losartan together with 5% NaCl (12.5 μg/5 μl/hr). After 14 days catheters were inserted into femoral artery and femoral vein for measurement of blood pressure (BP) and heart rate (HR) and for intravenous infusions respectively. All surgical procedures were performed under ketamine (100 mg/kg i.p.) and xylazine (10 mg/kg i.p.) anesthesia. After the implantation of catheters baroreflex was pharmacologically evaluated in conscious freely moving animals by administration of phenylephrine (i.v. from 20 up to 200 μg/kg/min) and sodium nitroprusside (i.v. from 20 up to 200 μg/kg/min) to induce a ramp increase and decrease of BP respectively. Subsequently autonomic ganglia were blocked with hexamethonium i.v. (20 mg/kg) and measurements of BP and HR continued. CSF was collected from cisterna magna before euthanasia of animals. Results: Infusions of 5% NaCl solutions resulted in higher concentration of sodium ions in CSF than in the plasma, while isoosmotic saline did not elevate CSF sodium concentration. The blockade of autonomic ganglia resulted in decrease of BP and increase in HR, which were similar in all groups. Baroreflex was blunted in rats receiving ICV infusion of hyperosmotic saline in comparison to control group. Intracerebroventricular administration of losartan restored sensitivity of baroreflex. Conclusions: Present results indicate that chronic ICV infusion of hyperosmotic saline desensitizes arterial baroreflex and this is partially mediated by AT1 receptors for angiotensin II.