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, we proposed a role for it in the development of primary hypertension. In this study, we screened for hypertension-related genes expressed in the NTS of spontaneously hypertensive rats (SHR). Three- and 18-week-old male SHR and their progenitor strain, Wistar-Kyoto rats (WKY) (all humanely killed), were used. cDNA microarray analysis was performed to find differentially expressed genes in the NTS between SHR and WKY. Signals exhibiting >2 difference between these strains were selected for further analysis using real-time RT-PCR. From 14,815 genes, 22 genes showed a greater expression in young (pre-hypertensive) and adult (hypertensive) SHR relative to WKY, whereas two other genes were down-regulated. So far, 4 genes have been proven to be differentially expressed using real-time PCR. One of these is junctional adhesion molecule-1 (JAM-1), which is highly expressed in both pre-hypertensive (n=4) and hypertensive SHRs (n=6) compared to WKY (young, n=4; adult, n=6). In the NTS of adult WKY (n=5), JAM-1 protein was exogenously expressed by using a recombinant adenoviral vector and cardiovascular variables were chronically measured using an automated computer analysis package (Waki et al. 2004). 7 days after viral injection, systolic pressure was significantly increased (119±4 vs 133±4 mmHg, p<0.01) while spontaneous baroreflex gain did not change (1.18±0.15 vs 1.56±0.30 ms mmHg^-1, p=0.21). Our data suggest that gene expression in the NTS is inherently different between SHR and WKY and that these differences are not secondary to the hypertension. One of differentially expressed genes – JAM-1 – appears important for controlling set point of arterial pressure. We conclude that over expression of JAM-1 may contribute to the hypertensive phenotype of the SHR.