Characterization of feline gastroduodenal junction by neural and hormonal stimulation.

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Abstract
The response of the feline gastroduodenal (GD) junction to vagal and hormonal stimulation was studied in vivo with an anchored manometric catheter. Pressure-diameter curves indicate that there is a short high-pressure zone at all probe diameters tested. Basal tone was unaffected by atropine and hexamethonium alone or in combination, by propranolol and by tetrodotoxin (TTX). It was decreased by phentolamine. The GD junction responded with relaxation to electrical stimulation of the peripheral end of the vagus nerve. This relaxation was reduced by hexamethonium alone or in combination with atropine and was abolished by TTX. It was not altered by .alpha.- or .beta.-adrenergic antagonists. Relaxation of the GD junction also was produced by direct electrical field stimulation of the junction wall. This relaxation was not affected by a combination of hexamethonium and atropine and was only abolished by TTX. The GD junction responded with contraction to electrical stimulation of the central end of the vagus nerve. This contraction was inhibited by a combination of atropine and hexamethonium and completely abolished by phentolamine and TTX. Cholecystokinin usually caused relaxation of the GD junction, whereas pentagastrin produced contraction only in 1/3 of the experiments. A structure that behaves like a sphincter may exist at the gastroduodenal junction.