Junctional adhesion molecule-1(JAM-1, or the F11 receptor) is a transmembrane protein located at the inter-cellular junctions of endothelial and epithelial cells (Martìn-Padura et al. 1998). Real-time RT-PCR revealed that JAM-1 mRNA was up-regulated in the nucleus tractus solitarii (NTS) of the spontaneously hypertensive rat (SHR) and young pre-hypertensive SHR compared with age-matched normotensive Wistar-Kyoto (WKY) rats (Waki et al. 2007). Here, we sought to compare JAM-1 levels in SHR with other rat models of hypertension. Male WKY, SHR, stroke-prone SHR (SP-SHR) and Wistar rats made hypertensive by renovascular occlusion (Goldblatt: 2 kidney 1 clip model) (n=6 for all groups) were overdosed with pentobarbital and perfused with Bouin’s solution. The brains were harvested and immunostained with goat anti-JAM-1 (1:200) antibody overnight, followed by incubation with biotinylated donkey anti-goat (1:500) for 1.5h and avidin-FITC (1:500) for 1h. JAM-1 immunofluorescence in the NTS was analysed using Image-Pro Plus 6.0 software on images obtained with a Leica confocal microscope. Fluorescence intensity of JAM-1 in WKY was 148±23 (units/section, mean±SEM), but up regulated to 433±72 (units/section, P<0.05) in SHR and higher in SP-SHR (720±89 units/section, P<0.01). JAM-1 was also up regulated in pre-hypertensive 3 week old SHR (144±22 vs 360±47, units/section, P<0.05). In Goldblatt rats (3 weeks post-surgery) arterial systolic blood pressure measured with radio-telemetry (anaesthetic for Goldblatt clamping and transmitter implantation was a mixture of ketamine hydrochloride (50%), medetomidine hydrochloride (30%) and 0.9% saline (20%) (0.2ml/300g, i.p.) followed after surgery with 10% atipamezole hydrochloride (1.5ml/kg, i.m.)) increased from 124±5 to 159±2 mmHg (mean±SEM, P<0.05, ANOVA) and was associated with enhanced JAM-1 immunofluorescence in NTS (381±49 vs. 138±17 units/section in control, P<0.05). When arterial pressure reached a plateau at 6 weeks (211±2 mmHg), JAM-1 immunofluorescence in NTS was not increased further (P<0.05). We next assessed whether up regulation of JAM-1 was specific to the brain. WKY, SHR, SP-SHR, pre-hypertensive SHR and Goldblatt rats (male, n=4 each group) were anaesthetised with halothane (5%) and decapitated. Brainstem blood vessels were isolated by ultracentrifugation (Mrsulja et al. 1976) along with tissues from lung, liver, kidney, spleen and heart. In all animal groups, JAM-1 protein levels were higher in all organs studied as determined by western blotting (P<0.05, ANOVA). These data indicate that up regulation of JAM-1 is a generalised phenomenon associated with early and pre-hypertensive stages of both genetic and renovascular hypertension and further supports its possible causative role in this pathological condition and, hence, as a novel prognostic indicator.