Nitric oxide and prostanoids participate in cerebral vasodilation elicited by electrical stimulation of the rostral ventrolateral medulla.

We investigated, using laser-Doppler flowmetry, whether nitric oxide (NO)- and/or indomethacin (IND)-sensitive mechanisms mediate the elevations of regional cerebral blood flow (rCBF) elicited by electrical stimulation of the rostral ventrolateral medulla (RVL) in the anesthetized spinalized rat. Stimulation of the RVL for 10 s caused increased rCBF in the frontal cortex by 31% (n = 46), peaking at 22 s and persisting for up to 8 min. Intravenous L-nitro-NG-arginine (NNA) dose dependently and reversibly increased arterial pressure and reduced basal and evoked rCBF to 74 and 54% of the control, respectively (p < 0.05; n = 7). Superfused over the cortex, NNA dose dependently reduced only the evoked elevations of rCBF, to 39% of the control (p < 0.05; n = 6). Intravenous IND decreased the basal rCBF dose dependently and decreased the elevations evoked from the RVL by 38% (p < 0.05), but IND was without effect when superfused. Combined, the effects of intravenous NNA and IND summated, reducing rCBF by 70%. However, when NNA and IND were superfused together, the inhibition of the evoked vasodilation was comparable to that elicited by NNA alone. We conclude that the elevation in rCBF elicited from the RVL is partially mediated by (a) NO synthesized locally in the cortex in response to an afferent neural signal and (b) an IND-sensitive mechanism, probably a product of cyclooxygenase, located in larger cerebral arteries, in response to a retrograde vascular signal resulting from increased blood flow within the brain.