Neurogenic vasodilation of dural blood vessels is not mediated by cholinergic transmission in the anaesthetised rat.

Dural vessel dilation induced by activation of trigeminal sensory fibres may be responsible for some component of the migraine attack. The presence in some patients with migraine and cluster headache of clinical features, such as lacrimation, suggests cranial parasympathetic activation and poses the question as to whether neurogenic meningeal dilatation has a cholinergic component. Rats were prepared in order to record on-line the diameter of a middle meningeal artery branch through a closed cranial window using an intravital microscope coupled to a video dimension analyser. Acetylcholine (1 microg, intravenously, i.v.) was administered before and after muscarinic receptor inhibition (n=5) with scopolamine (2 mg/kg, i.v.) or nicotinic receptor inhibition (n=6) with mecamylamine (4 mg/kg, i.v.). Further vasodilation was induced by electrical stimulation of the cranial window surface before and after muscarinic receptor inhibition with i.v. scopolamine (n=8). The mean dural vessel percentage increase caused by acetylcholine stimulation was significantly different before and after muscarinic receptor inhibition (P=0.045). Moreover, there was no difference between the post receptor inhibition values and those obtained after vehicle infusion (P=0.431). In contrast, no difference was detected in the effect of acetylcholine before and after nicotinic receptor inhibition (P=0.688). In the second experiment, where the effect of muscarinic receptor inhibition on the neurogenic dilation model was assessed, no significant difference was demonstrated (P=0.538). Cholinergic dilation of the rat dural arteries is mediated by muscarinic receptors, but this mechanism does not play a significant role in the rat dural vessel dilation induced by closed cranial window electrical stimulation.