The nucleus tractus solitarii (NTS) is a brainstem region involved in the regulation of arterial pressure and the baroreceptor reflex. Hence, any change in gene expression in NTS could affect blood pressure (BP). We have already shown that cDNA microarray analysis of the NTS indicates that leukotriene B4 12-hydroxydehydrogenase (LTB4 12-HD) is down-regulated in the spontaneous hypertensive rat (SHR) compared to its normotensive control (Wistar-Kyoto or WKY; Waki et al. 2004). As LTB4 12-HD breaks down leukotriene B4 (LTB4), we propose that it is up-regulated in the NTS of the SHR. LTB4 acting via BLT1 receptors is a major chemoattractant of leukocytes to the endothelium (Yokomizo et al. 2001). As leukocyte adhesion in the microvasculature of the NTS is prevalent in the SHR, and when induced causes hypertension (Waki et al. 2007), we suggest that excessive LTB4 in NTS in the SHR may contribute to the maintenance of the high BP in this animal model. To assess whether chronic systemic blockade of BLT1 receptors in the SHR exerts an anti-hypertensive effect. The procedures were carried out according to the Animals (Scientific Procedures) Act 1986. Under general anaesthesia adult male SHR and WKY rats weighing ~350g were implanted with a radio-telemetry transmitter (Data Sciences International) to record chronically arterial pressure (mixture of ketamine, 60 mg kg^-1 and medetomidine, 250 μg kg^-1, i.p). For details of the surgical procedure see Waki et al. (2003). Following surgery anaesthesia was reversed with a subcutaneous injection of atipamezole (1 mg kg^-1) and animals were allowed to recover for one week. Baseline BP was recorded in the conscious rats for at least 3 days before chronic oral administration of a BLT1 receptor antagonist (CP-105696, 1 mg/ml in 1.25% DMSO in drinking water) for 4 weeks. Fluid intake was monitored throughout the course of the experiment. In SHR, CP-105696 induced a substantial reduction in systolic blood pressure (SBP; peak response -23 ± 6 mmHg; one way ANOVA repeated measures and Dunnett’s multiple comparison test, P<0.01, n=8) that occurred 11 ± 1.6 days after administration. After the peak fall in SBP, it recovered partially but remained significantly lower relative to baseline levels (i.e. -13 mmHg; P<0.05, n=7) until the end of the recording time (27 days post drug administration). In contrast, in WKY rats inhibiting BLT1 receptors was ineffective in altering SBP pressure (n=5). When vehicle (1.25% DMSO) alone was added to the drinking water there was no change in arterial pressure (n=2). These data indicate that blockade of BLT1 receptors reduces arterial pressure in the SHR but not WKY rats. Our finding is consistent with the notion that the hypertension in the SHR is dependent, in part, on inflammation of the vasculature, which may include that within NTS and other brain regions controlling vasomotor tone.