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Despite the increasing number of publications devoted to the cerebrovascular role of NO, its precise influence in awake animals is still poorly characterized. The effect of nitric oxide synthase (NOS) inhibition on the cerebrovascular CO 2  reactivity was therefore studied in conscious rats. Regional CBF was measured using the [ 14 C]iodoantipyrine technique and brain tissue sampling. The CO 2  reactivity was determined 60 min after administration of 30 mg kg −1  N ω -nitro-l-arginine methyl ester (l-NAME). Blockade of NOS by l-NAME significantly decreased CBF in all 11 brain regions studied (−17 to −49%) and increased arterial pressure from 117 ± 12 to 147 ±11 mm Hg. In control conditions, CO 2  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. Following l-NAME injection, the reactivity to hypercapnia was significantly attenuated in all structures, the magnitude of the reduction ranging from 57% in the medulla to 74% in the cerebellum. This result shows that NO is an important mediator of the hypercapnic vasodilation in the conscious rat.

Widespread Attenuation of the Cerebrovascular Reactivity to Hypercapnia following Inhibition of Nitric Oxide Synthase in the Conscious Rat