PMC:4536246 / 18097-18522 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/4536246","sourcedb":"PMC","sourceid":"4536246","source_url":"https://www.ncbi.nlm.nih.gov/pmc/4536246","text":"The present data suggest that ADMA accumulates in the brain after GTN administration via the inhibition of DDAH-1. This latter may represent a compensatory response to the excessive local availability of NO, released directly by GTN or synthetized by nNOS. These findings prompt an additional mediator (ADMA) in the modulation of NO axis following GTN administration and offer new insights in the pathophysiology of migraine.","tracks":[]}