Introduction: A growing body of evidence shows that brain TNF has prohypertensive effects on the regulation of arterial blood pressure [1,2]. Neuronal nitric oxide synthase (nNOS) participates in the central control of the arterial blood pressure and baroreflex, exerting antihypertensive effects in hypertensive animals [3]. TNF stimulates expression of hypothalamic nNOS and induces synthesis of nitric oxide [3]. Aim: We checked how TNF infused into the cerebral ventricles affects arterial blood pressure, heart rate and spontaneous baroreflex sensitivity, and whether TNF actions are dependent on nNOS in normotensive rats. Methods: We instrumented 28 adult male Sprague-Dawley rats with arterial catheter and intracerebroventricular (ICV) canula under anesthesia with intraperitoneal ketamine (100 mg/kg b.w.) and xylazine (10 mg/kg b.w.). We did hemodynamic measurements in freely moving conscious rats during hourly ICV infusion of either: 1) saline (5 microl/hr); 2) TNF (200 ng/5 microl/hr); 3) nNOS inhibitor – 7-nitroindazole sodium salt (7-NI) (20 microg/10 microl/hr); 4) or TNF together with 7-NI (200 ng and 20 microg/10 microl/hr, respectively). We analysed mean arterial blood pressure (MABP), heart rate (HR) and spontaneous baroreflex sensitivity (sBRS) evaluated by the sequence method. The data were analysed with repeated measures one-way and two-way ANOVAs. Results: ICV infusion of TNF resulted in a significant increase in MABP, a transient increase in HR and a decrease in sBRS in comparison to pre-infusion values (one-way ANOVA, p<0.05) and to control and 7-NI infused rats (two-way ANOVA, p<0.05). ICV infusion of 7-NI had no effect on MABP, HR, or sBRS. ICV infusion of TNF with 7-NI significantly increased MABP without changes in HR in comparison to pre-infusion values (one-way ANOVA, p<0.05) and to control and 7-NI infused animals (two-way ANOVA, p<0.05). Coadministration of TNF and 7-NI restored sBRS (two-way ANOVA, p<0.05). Conclusions: Intracerebroventricularly infused TNF increases MABP and blunts sBRS. The pressor effect of TNF appears to be independent of nNOS activity in the brain. However, our results suggest that neuronal NOS participates in the depressor effect of TNF on sBRS.