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Department of Pharmacology, Faculty of Veterinary Medicine, Hokkaido University, Sapporo, Japan.

1. Gastric vasodilatation, relaxation, and vasoactive intestinal peptide (VIP) output in response to vagal stimulation were studied in anaesthetized dogs. 2. Stimulation of the peripheral end of the vagus nerve (10 Hz, 40 V, 0.5 ms) normally evoked a gastric contraction, but caused relaxation in atropinized dogs. There was no detectable difference between the electrical thresholds for activation of the vagal preganglionic excitatory and inhibitory motor fibres. 3. Vagal stimulation also evoked gastric vasodilatation, which was blocked by hexamethonium but not by combined muscarinic and adrenergic blockade. Vagal fibres evoking vasodilatation had higher thresholds to electrical stimulation than those evoking motor responses. 4. Both gastric motor responses to vagal stimulation increased with increasing frequency up to 10 Hz and a plateau between 10 and 40 Hz, but the vasodilator response was significantly reduced above 20 Hz. Vagal stimulation at 10 Hz caused an increase in gastric venous VIP output which was significantly reduced at 40 Hz. 5. Low-intensity vagal stimulation (10 Hz, 40 V, 0.05 ms) elicited gastric relaxation (40% of a maximum), with no release of VIP or gastric vasodilatation. 6. It is concluded that release of VIP in response to stimulation of the vagal innervation to the stomach in the dog is primarily vasodilating in action.

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