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Since the identification of the gas nitric oxide (NO) as the endothelial-derived relaxing factor, NO has increasingly been recognized as being involved in numerous physiological and pathophysiological processes, in particular those related to inflammation and blood flow. NO can be synthetized by three isoforms of nitric oxide synthase (NOS): nNOS (neuronal NOS) and eNOS (endothelial NOS), which are both constitutive, Ca 2+ -dependent enzymes, and iNOS (inducible NOS), which produces large amounts of NO in inflammatory reactions ( ).
Since the first report of showed the protective effects of NOS inhibitors in mouse stroke models, the potential of NOS inhibitors in the treatment of neurological injuries has been emphasized not only in stroke but also in traumatic brain injury (TBI) ( ). While the role of NO in TBI pathophysiology—as in stroke—is widely accepted, inconsistent results have been reported regarding the effect of NOS inhibitors in experimental TBI, thus confirming the double-edged role of NO in brain injury ( ). As a result, NOS inhibitors are not currently in clinical development for the treatment of stroke or—with one exception—TBI.
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