Human essential hypertension is a complex polygenic trait with underlying genetic components that remain unknown. Since the brainstem structure – the nucleus of the solitary tract (NTS) – is a pivotal region for regulating the set-point of arterial pressure (e.g. Doba & Reis, 1974), we proposed a role for it in the development of primary hypertension. Recently, we identified that junctional adhesion molecule-1 (JAM-1; a leukocyte/platelet adhesion molecule) was over expressed in endothelial cells in the NTS of SHR compared to normotensive Wistar-Kyoto rat (WKY; Waki et al. 2005). Moreover, over expression of JAM-1 by adenoviral gene delivery in the NTS induced hypertension in the WKY indicating that JAM-1 may be pro-hypertensive (Waki et al. 2005). In the present study, we have assessed the level of gene expression of other major leukocyte/platelet adhesion molecules and cytokines in the NTS of SHR relative to WKY. The NTS was micro-dissected from 15-week-old male SHR (n=5) and WKY (n=5) rats. Total RNA was extracted and real-time RT-PCR was performed. Expression of target genes relative to an internal control, β-actin, was derived in each sample using the comparative (2^-ΔΔCT) method. Data were expressed in fold differences against the average value of WKY. Gene expression of monocyte chemoattractant protein -1 (MCP-1) was significantly higher in the NTS of SHR (SHR: 1.70±0.14, n=5; WKY: 1.08±0.21, n=5, p<0.05) while inter-leukin-6 (IL-6) was significantly lower in the NTS of SHR compared to the WKY (SHR: 0.41±0.12, n=5; WKY: 1.03±0.12, n=5, p<0.01). In contrast, expression of adhesion molecules including: intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and junctional adhesion molecule-3 were not different. Our data suggest that the NTS of the SHR exhibits a specific inflammatory state. The high expression level of mRNA JAM-1 and MCP-1 and lowered IL-6 in the NTS of the SHR is a unique characteristic. Whether this expression profile contributes to the hypertensive state via alteration of neuronal circuitry regulating cardiovascular autonomic activity remains to be resolved.