Role of nitric oxide synthase-containing vascular nerves in cerebrovasodilation elicited from cerebellum.

We studied whether the increases in cortical cerebral blood flow (CBF) elicited by stimulation of the cerebellar fastigial nucleus (FN) are attenuated by systemic administration of inhibitors of nitric oxide synthase (NOS) and, if so, whether NOS-containing perivascular nerves arising from the sphenopalatine ganglia (SPG) are the source of NO during FN stimulation. Rats were anesthetized (1-3% halothane) and artificially ventilated. The FN or the pontine reticular formation (PRF) was stimulated electrically through a stereotaxically implanted microelectrode. To eliminate the elevation in arterial pressure (AP) elicited by FN or PRF stimulation the cervical spinal cord was transected and AP was maintained by intravenous phenylephrine. CBF was measured by a laser-Doppler probe placed over the parietal cortex. Systemic administration of the NOS inhibitor N omega-nitro-L-arginine methyl ester (L-NAME; 5-40 mg/kg) reduced resting CBF, an effect that was maximal at 10 mg/kg (-30 +/- 4%; n = 6; P < 0.003, analysis of variance). L-NAME, but not its inactive isomer D-NAME, attenuated the increases in CBF elicited by FN stimulation or hypercapnia in a dose-dependent fashion (10-40 mg/kg). At 40 mg/kg, the response to FN stimulation was reduced by 80 +/- 6% (n = 6; P < 0.05) and that to hypercapnia was reduced by 70 +/- 9% (P < 0.05). In contrast, the increases in CBF elicited by PRF stimulation were not affected (10-40 mg/kg; P > 0.05; n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)