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Abstract
Background: The involvement of nitric oxide (NO) in vagal control and vasoactive intestinal polypeptide (VIP)-induced effects on antral motility was studied using isolated perfused preparations of porcine gastric antrum with intact vagal innervation. Methods: The presence of NO and VIP-producing neurons was studied using immunohistochemistry and histochemical techniques. Widespread, but not total, co-localization of NO and VIP immunoreactivity was found in the submucosa and in the muscle layers. Results: Electrical stimulation of the vagus nerves for 5 r min (8 r Hz, 10 r mA, 4 msec) increased the motility index from 2.47 ± 0.44 to 11.50 ± 2.02 ( n r = r 5). This effect was not influenced by the two NO synthase inhibitors N-nitro- L -arginine methyl ester (10 m 4 r M) and N G -nitro- L -arginine (10 m 5 r M). However, infusion of inhibitors increased the spontaneous motility index from 2.40 ± 0.08 to 5.36 r ± 1.08 ( P r < r 0.05) and 3.05 ± 1.10 to 4.14 ± 1.04 ( P r < r 0.05), respectively. The addition of L -arginine reversed this effect. Infusion of VIP 2 r × r 10 m 9 r M decreased the motility index from 2.32 ± 0.43 to 1.32 ± 0.27 ( P r < r 0.05), an effect that was preserved during NO synthase inhibition. Electrical vagus stimulation increased the release of VIP to the venous effluent, an effect that persisted during NO synthase inhibitors. Conclusion: We conclude that NO-producing nerves seem to have a tonic inhibitory action on the porcine antral motility, but are not involved in the motor effects of vagal stimulation or VIP infusion.