The pterygopalatine ganglion (PPG) is the major source of cerebrovascular parasympathetic innervation. Stimulation of parasympathetic nuclei releases nitric oxide (NO) from postganglionic nitrergic nerves, inducing cerebral vasodilatation (1). It has been shown, in young (Y) rats, that PPG stimulation induces significant cerebral vasodilatation (increase in cerebrovascular conductance; CVC) resulting in increases in cerebral blood flow (CBF), with no change in arterial blood pressure (ABP) (2). Our findings in Y rats agree with these observations. However, we have evidence these dilator fibres are functionally important. We showed the increase in cerebral blood flow (CBF) beyond the upper limit (UL) of autoregulation (in response to increased ABP) is associated with a vasodilatation (fall in cerebrovascular resistance; CVR). Infusion of the NO synthase inhibitor L-NAME prevented the UL being reached and so abolished the dilatation seen at a comparable ABP. These observations suggest an active, NO-mediated dilatation as opposed to a pressure-passive increase in CBF when the UL is reached in Y rats. This increase in CBF and fall in CVR at the UL was blunted in old (O) compared to Y rats. We therefore hypothesise that the increase in CBF beyond the UL may be mediated by an increase in parasympathetic, nitrergic nerve activity to the cerebral vessels, and that this mechanism is impaired with age. In Alfaxan-anaesthetised (12-30mg.kg.hr-1 i.v.), male O Wistar rats (52-58 weeks old, n=8), we isolated and stimulated the PPG at 3, 10, 30 and 60Hz (2-4V for 90 seconds) before and after infusion of L-NAME (10mg.kg-1 i.v.). Data is presented as mean±SEM. The responses were blunted in O compared to Y rats. The higher frequencies induced significant increases in CBF, with a maximum increase of 0.36±0.07ml.min-1* at 10Hz (paired t-test, P<0.05). However, this was associated with a concomitant increase in ABP of 17±3mmHg* (paired t-test, P<0.05) and only a small, non-significant, increase in CVC (0.019±0.002 to 0.02±0.002ml.min-1.mmHg, paired t-test, P>0.05). Infusion of L-NAME significantly reduced the increase in ABP in response to PPG stimulation at 10Hz; CVC remained unchanged, resulting in a reduced increase in CBF. These data suggest that PPG-induced dilatation is substantially blunted in O rats, the ABP increase accounting for the increase in CBF. We suggest that the increase in CBF seen beyond the UL is an active, NO-mediated dilatation, caused by nitrergic, parasympathetic nerve activation. This may be part of a pressure-release safety mechanism in response to increases in ABP, which may otherwise compromise the cerebral vasculature. This mechanism appears to be blunted in old rats, which may have implications for the increased risk of haemorrhagic stroke associated with ageing.