To determine whether splanchnic nerves relax the stomach by direct or indirect mechanisms, ramp inflations of the stomach, section and electrical stimulation of the vagus and greater splanchnic nerves, and step inflations of the duodenum were used. A high threshold, sustained inhibition of the gastric pressure response to ramp inflation was mediated by the vagus. Prior splanchnectomy increased vagal inhibition. The greater splanchnic nerves had no effect on gastric responses to inflation, although after vagotomy they were shown to be mediators of a low threshold, powerful but transient inhibition of the stomach. This was not dependent on intrinsic neurones with nicotinic receptors. Electrical stimulation of the greater splanchnic nerves produced a relaxation of the stomach, the magnitude of which was determined by resting pressure. Splanchnically mediated relaxation was not abolished by atropine, nor was it reduced by concurrent vagal stimulation. At submaximal levels of vagal stimulation the two nerves had a partially additive effective on relaxation. Duodenal inflation had an effect on intracorpus pressure similar to that of electrical stimulation of the greater splanchnic nerves on intragastric pressure. Reflex relaxation of the corpus evoked by duodenal distension was decreased by atropine but greatly increased by atropine coupled with vagotomy. These changes were caused by variations in resting pressure. It was concluded that the principal effect of splanchnic nerves on mean gastric pressure is direct and does not depend on inhibition of cholinergic neurones either centrally or peripherally. Evidence is presented for central interactions between the vagus and the greater splanchnic nerves in the anaesthetized ferret.
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