WIDESPREAD ATTENUATION OF THE CEREBROVASCULAR REACTIVITY TO HYPERCAPNIA FOLLOWING INHIBITION OF NITRIC-OXIDE SYNTHASE IN THE CONSCIOUS RAT

Despite the increasing number of publications devoted to the cerebrova scular role of NO, its precise influence in awake animals is still poo rly characterized. The effect of nitric oxide synthase (NOS) inhibitio n on the cerebrovascular CO2 reactivity was therefore studied in consc ious rats. Regional CBF was measured using the [C-14]iodoantipyrine te chnique and brain tissue sampling. The CO2 reactivity was determined 6 0 min after administration of 30 mg kg(-1) N-omega-nitro-L-arginine me thyl ester (L-NAME). Blockade of NOS by L-NAME significantly decreased CBF in all 11 brain regions studied (-17 to -49%) and increased arter ial pressure from 117 +/- 12 to 147 +/- 11 mm Hg. In control condition s, CO2 responsiveness ranged from 1.3 +/- 0.4 in the hypophysis to 6.4 +/- 0.6 ml 100 g(-1) min(-1) mm Hg-1 in the parietal cortex. Followin g L-NAME injection, the reactivity to hypercapnia was significantly at tenuated in all structures, the magnitude of the reduction ranging fro m 57% in the medulla to 74% in the cerebellum. This result shows that NO is an important mediator of the hypercapnic vasodilation in the con scious rat.