A diet containing high load of salt is considered as one of the important contributing factors 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, which rearranges central control of the cardiovascular system (1). Recently proinflammatory cytokines (PICs) acting in the central nervous system were recognized as an important player in the pathogenesis of hypertension (2). Hyperosmotic conditions are known to induce synthesis of PICs (3). In the present study we seeked to find ouf if centrally released PICs contribute to changes in the control of circulatory system induced by intracerebroventricular (ICV) infusion of hyperosmotic saline. To inhibit PICs production we decided to use a tetracycline antibiotic, minocycline, which inhibits release of PICs from microglial cells. 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 ICV infusion of either isoosmotic saline (0.9% NaCl, 5 μl/hr), hyperosmotic saline (5% NaCl, 5μl/hr) or minocycline (5 μg/hr) together with hyperosmotic saline (5% NaCl, 5μl/hr). After 14 days catheters were inserted into femoral artery and femoral vein for measurement of BP and HR and for intravenous infusions. All surgical procedures were performed under ketamine (100 mg/kg i.p.) and xylazine (10 mg/kg i.p.) anesthesia. 24-48hr after implantation of catheters we conducted measurements according to the following protocol: after baseline measurement of BP and HR, acute stressor was applied in the form of standarized air jet directed on the rat’s head. Then baroreflex was pharmacologically tested by administration of phenylephrine i.v. (from 20 up to 200 μg/kg/min) in order to produce a ramp increase of BP. After return of BP and HR to resting values nitroprusside was infused i.v.(from 20 up to 200 μg/kg/min) to generate a ramp decrese of BP. Subsequently autonomic ganglia were blocked with hexamethonium i.v. (20 mg/kg) and measurements of BP and HR continued. The increase of BP in response to air jet stress differed insignificantly between treatments. The blockade of autonomic ganglia resulted in similar decrease of BP and increase in HR in all groups. Baroreflex was blunted in rats receiving ICV infusion of hyperosmotic saline in comparison to control group. Treatment with minocycline restored sensitivity of baroreflex. In conclusion these results show that centrally administered minocycline prevents desensitization of baroreflex caused by chronic ICV infusion of hyperosmotic saline.