Normal Radial Artery Dilatation During Reactive Hyperaemia in Migraine without Aura

Abstract

Increasing evidence suggests that nitric oxide (NO) plays a role in migraine pain. Thus, the NO donor glyceryl trinitrate provokes migraine attacks in sufferers and a greater dilatation of large arteries than in controls. Physiological NO-mediated dilatation of large arteries might therefore be abnormal in migraine. Recently an ultrasound method for the detection of shear stress stimulated endothelial NO release in large arteries in man has been described. Using this method we compared radial artery dilatation during reactive hyperaernia in 12 female sufferers of migraine without aura and 12 age- and sex- matched healthy subjects. No group differences were detected in these responses (peak dilatation 111 ± 2% (mean ± SEM) of baseline in migraineurs and 112 ± 3% of baseline in the healthy control group, p = 0.79). These results indicate that shear stress stimulated endothelial NO release is normal in peripheral conduit arteries in patients suffering from migraine without aura. It remains to be settled whether the same is true in extra- and intracranial arteries.