VIP as a mediator of hexamethonium-sensitive, atropine-resistant vasodilation in the cat tongue.

Abstract

Electrical stimulation (10 V, 0.2 ms) of the chorda‐lingual nerve caused a biphasic vasodilatory response in the cat tongue with an initial phase which was most marked at low frequencies and a maintained phase which increased with frequency. Simultaneously, there was a VIP release as indicated by a marked increased VIP output from the tongue. VIP output increased with time of stimulation and was most pronounced at high frequencies. Atropine abolished the initial phase of vasodilation at low frequencies as well as reduced this phase at medium frequencies. At high frequency stimulation (15 Hz), the vasodilation was still somewhat reduced by atropine but in contrast to the cat submandibular salivary gland, the duration of the vasodilatory response did not increase after atropine. Furthermore, atropine did not increase VIP output from the tongue during nerve stimulation. Hexamethonium completely abolished VIP release as well as most of the vasodilation upon stimulation of the chorda‐lingual nerve. The remaining vasodilation may be due to antidromic stimulation of unmyelinated trigeminal sensory neurons, since it was present when using high threshold stimulation parameters (10 V, 5 ms). Local intra‐arterial infusion of acetylcholine or VIP caused a marked vasodilation of the tongue. Also substance P infusion induced a vasodilatory response. The response to acetylcholine was atropine sensitive, while the effects of VIP and substance P were atropine‐resistant. Combined infusions of VIP and acetylcholine had an additive effect on vasodilation. In conclusion, the present data suggest that low threshold chorda‐lingual nerve stimulation induced a release of both acetylcholine and VIP from postganglionic neurons in the tongue. The contribution by these two agents in the vasodilatory response may then depend upon time and frequency of stimulation. In contrast to the VIP nerves in the submandibular gland, no evidence suggests that VIP release from vascular nerves in the tongue is affected by atropine. High threshold stimulation also induces antidromic vasodilation possibly mediated via substance P release.