• L Lundblad, A Anggård, and J M Lundberg.
• Acta Physiol. Scand. 1983 Sep 1; 119 (1): 7-13.

AbstractHigh threshold stimulation of the trigeminal nerve in sympathectomized cats caused an atropine and hexamethonium resistant vasodilation in the nasal mucosa. Stimulation of efferent parasympathetic neurons to the nose caused a partially atropine sensitive vasodilation which was abolished by hexamethonium. Combined trigeminal and parasympathetic nerve stimulation did not reveal any obvious functional interactions between these two systems. Local intra-arterial infusions of substance P, VIP and acetylcholine caused a dose dependent vasodilation in the nasal mucosa. The relative vasodilatory potencies were substance P greater than to VIP greater than acetylcholine. Local infusions of capsaicin, known to release substance P from nerve endings, caused a marked longlasting biphasic vasodilation which was atropine and hexamethonium resistant. In conclusion, the present findings illustrate the presence of two vasodilator mechanisms of different nervous origin in the nasal mucosa. The trigeminal response is probably mediated via release of substance P, while the parasympathetic effect seems to be caused by acetylcholine and VIP.

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