Our recent evidence suggests that elevating cerebral vascular resistance in normotensive rats produces hypertension (Paton at el (2011). We tested whether elevating cerebrovascular resistance by permanent occlusion of 3 cerebral arteries supplying the brain (3 vessel occlusion, 3VO: right carotid and both vertebral arteries) in spontaneously hypertensive rats (SHR) would produce a larger elevation in arterial pressure as they already have high cerebrovascular resistance. Male SHR (≥250g) were anaesthetized with ketamine (60mg/kg) and metadomidine (250µg/kg) i.p. The level of anaesthesia was frequently checked during the procedure using the pinch reflex. Body temperature was maintained at 37°C using a heat blanket. The animals were recovered from anaesthetic with a subcutaneous injection of atipamezole (1mg/kg) and given buprenophine (0.15mg/kg) for pain relief as needed. Post surgery animals were housed individually, given standard rat chow and water ad libitum and kept in a climate controlled room on a 12 hour light/dark cycle. For BP monitoring, a DSI radiotelemetry implant was placed in the descending aorta. Following surgery rats were allowed to recover for at least 7 days before starting baseline BP recordings. For 3VO, the right common carotid and both vertebral arteries were occluded. Sham animals underwent the same surgery without occlusion of vessels. Cerebral vessels were studied 15-31 days after 3VO. 3VO elicited a rapid and significant increase in systolic BP (17±2(SEM) mmHg) from baseline compared to sham controls (3VO n=7, sham control n=6, p<0.001, unpaired T-test) lasting approximately 3 days after which BP returned towards baseline. The peak pressor response in SHR was larger than that seen in normotensive rats (~15mmHg, Paton et al (2011)). Histological examination revealed that the diameter of the left vertebral artery, ventral medial spinal artery and right posterior communicating artery were increased significantly in the 3VO group by 19.3% (3VO n=9 vs. sham n=10, p<0.05), 56% (3VO n=6 vs. sham n=8, p<0.01) and 74.7% (3VO n=6 vs. sham n=4, p<0.01) respectively compared to the shams. In conclusion, our studies have provided further support of a neurovascular/cerebrovascular control of BP as occlusion of cerebral arteries feeding the brain results in a marked increase in BP, which is greater in SHR than normotensive rats. We propose that the vessel re-modelling is responsible for the lowering of BP after the initial pressor response post 3VO and permits an attempt to restore cerebral perfusion.