It is known that the cerebral vasculature is innervated with sympathetic fibres originating primarily from the superior cervical ganglion (SCG). However, the role that these sympathetic fibres play in control of the cerebral circulation remains controversial. Some evidence suggests a tonic sympathetic constrictor influence on cerebral blood flow (CBF) and a role in autoregulatory vasoconstriction in response to increases in arterial blood pressure (ABP) towards the upper limit (UL), giving protection of the blood brain barrier. Ageing is generally associated with impaired sympathetic functioning; involving changes in both innervation density and transmitter biosynthesis. But how this affects the cerebral circulation and autoregulation of CBF is unknown. We hypothesised that sympathectomy (sympX) would lower the UL in young (Y) rats, due to a reduced capacity for autoregulatory vasoconstriction. In old (O) rats, as this vasoconstriction may already be impaired, we hypothesised no effect of sympX on the UL, and also that the UL would be lower in O than intact Y rats. In Alfaxan-anaesthetised (12-30mg.kg.hr-1 i.v.), Y (6-8 weeks, n=7) or O (52-58 weeks, n=10), male Wistar rats, we isolated the SCG and performed bilateral sympX. Gross CBF was recorded from the common carotid arteries after external carotid ligation. Data is expressed as mean±SEM, and statistics used were paired (*) or unpaired (†) t-tests. P<0.05 was considered significant. In Y rats, bi sympX significantly increased basal CBF from 1.9±0.1ml.min-1, by 0.6±0.1ml.min-1*. In O rats, basal CBF was significantly higher than Y (2.9±0.3ml.min-1†) and bi sympX similarly and significantly increased CBF by 0.7±0.1ml.min-1*. Phenylephrine was then infused (0.1-200µg.kg.min-1 i.v.) to raise ABP and the autoregulatory UL was determined by dual-line linear regression analysis of CBF vs ABP. The gross UL after sympX in Y rats was higher than that in intact Y rats (178±3* vs 168±2mmHg). In O rats, the gross UL after sympX was significantly higher, or even abolished, compared to intact O rats (190±3* vs 180±3mmHg), and also when compared to Y rats; both intact and post-sympX. We propose that sympathetic fibres have a role in maintaining basal cerebrovascular tone, and that this is similar for Y and O rats. Further, sympathetic innervation appears to limit the autoregulatory UL in both Y and O rats, such that removal of sympathetic input raises the UL. The mechanism responsible for further vasoconstriction in the absence of sympathetic activity may be the myogenic response. Structural differences between the cerebral vessels of Y and O may therefore account for the higher UL in O.