Introduction: Tumour necrosis factor (TNF) is an archetypal proinflammatory cytokine implicated in cardiovascular diseases (1). A growing body of evidence shows that brain TNF is involved in blood pressure regulation and sympathoexcitation (2),(3). Neuroinflammation of the brain nuclei involved in the regulation of the cardiovascular system has been recognized as an important contributing factor to the pathogenesis of hypertension (4). The proinflammatory effects of TNF in the central nervous system are mediated by TNF type 1 receptors (TNFR1) (5). Aim: In the present study we checked if spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats differ in concentrations of TNF and its receptor TNFR1 in the key cardiovascular centres of the brain. Methods: We measured systolic blood pressure in adult male SHR (n=6) and WKY (n=6) rats with tail-cuff method. Then under anesthesia with urethane (1.5 g/kg b.w., i.p.), we collected blood and brains, which were snap frozen in liquid nitrogen immediately after euthanasia. Brains and serum were stored at -80°C for further analysis. We sectioned coronal slices of the brain in the brain matrix and isolated the hypothalamus (HTH), the rostral ventrolateral medulla (RVLM) and the nucleus of the solitary tract (NTS). After homogenization and centrifugation of the tissues, we used the enzyme-linked immunosorbent assays to determine concentration of TNF in the obtained supernatants of HTH, RVLM and NTS and concentration of TNFR1 in the precipitates of the respective areas. We also measured norepinephrine (NE), TNF and TNFR1 in serum. Student’s t-test was used for statistical analysis. Values are expressed as means ± SD. Results: SHR rats had significantly higher systolic blood pressure than WKY rats, 182±13 vs 142±19 mmHg (p<0.001). Protein expression of TNF in RVLM and NTS of SHR rats was significantly higher than in WKY rats, 2243±193 vs 1523±154 pg/g of tissue (p=0.001) and 2290±219 vs 1643±105 pg/g of tissue (p=0.002), respectively. Concentration of the cytokine in HTH and serum did not differ significantly between SHR and WKY rats. TNFR1 expression was significantly higher in NTS of SHR than in WKY rats, 5494±311 vs 4577±565 pg/g of tissue (p=0.029). There were no significant differences in concentration of TNFR1 in HTH, RVLM and serum between normotensive and hypertensive rats. Serum NE was 12.6 ± 2.0 ng/ml in SHR vs 3.8 ± 1.4 ng/ml in WKY rats (p=0.036). Conclusions: Our results show that expression of TNF is increased in the brainstem of SHR rats and this increase is accompanied by augmented expression of TNF type 1 receptor. Increased expression of both, the cytokine and its receptor, may provide a setting for inflammatory response contributing to the hypertensive milieu.