Competitive inhibition of nitric oxide synthase prevents the cortical hyperemia associated with peripheral nerve stimulation.
AUTOR(ES)
Northington, F J
RESUMO
With combined microdialysis and hydrogen clearance techniques for simultaneous local delivery of drugs and blood-flow measurement in the rat hindlimb sensory-motor cortex, we examined the role of nitric oxide in cerebral blood-flow regulation during sciatic nerve stimulation. Infusion of 1 mM nitric oxide synthase antagonist, N eta-nitro-L-arginine methyl ester (L-NAME), blocked the cortical blood-flow response to sciatic nerve stimulation (152 +/- 43 ml.min-1.100 g-1 of tissue in controls and 73 +/- 11 ml.min-1.100 g-1 in the presence of L-NAME; P less than 0.05). Addition of 10 mM L-arginine to the dialysate containing L-NAME partially restored the hyperemic response to nerve stimulation (125 ml.min-1.100 g-1). L-NAME also produced a decrease in baseline cerebral blood flow when compared with the control (66 +/- 14 ml.min-1.100 g-1 vs. 93 +/- 25 ml.min-1.100 g-1). We conclude that nitric oxide from activated neurons participates in the local regulation of cortical blood flow in response to sciatic nerve stimulation and also in the maintenance of basal cortical blood flow.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=49559Documentos Relacionados
- The response of the tremor of patients with Parkinsonism to peripheral nerve stimulation.
- Direct evidence of nitric oxide release from neuronal nitric oxide synthase activation in the left ventricle as a result of cervical vagus nerve stimulation
- Myeloperoxidase up-regulates the catalytic activity of inducible nitric oxide synthase by preventing nitric oxide feedback inhibition
- Macrophage Nitric Oxide Synthase Associates with Cortical Actin but Is Not Recruited to Phagosomes
- Dual inhibition of nitric oxide and prostaglandin production contributes to the antiinflammatory properties of nitric oxide synthase inhibitors.