Control of Gastric Motility Differs in the Proximal and Distal Stomach
The motility of the stomach, as in other smooth muscle portions of the gut, is under neurohumoral control. Fibers of the vagus nerve synapse on nerve cell bodies of the extensive gastric myenteric plexus and exert a high degree of control over gastric motility.
The effects of vagal stimulation on the proximal and distal regions of the stomach are opposite; in the proximal stomach, vagal activity suppresses muscular contractions and leads to adaptive relaxation, whereas in the distal stomach, vagal stimulation causes intense peristaltic activity. VagaI stimulation of distal antral motility is mediated by acetylcholine, but vagal inhibition of proximal stomach motility is not. The identity of the inhibitory mediator is not well established, but it may be vasoactive intestinal peptide.Vagal action on the stomach is stimulated by events occurring within the CNS, as well as within the stomach and intestine. The anticipation of food consumption causes vagal stimulation of the stomach and thus primes the stomach to receive a meal. Reactions of the GI tract that originate in the CNS in response to anticipated food intake are often referred to as the cephalic phase of digestion. Reactions to the cephalic phase are then augmented as food enters the stomach. In response to food in the stomach, vagal activity increases as sensory receptors in the stomach create a positive feedback loop.
The exact role of hormones in regulation of gastric motility is not completely established. Gastrin, which is secreted from cells in the gastric antrum, appears to enhance gastric motility. Cholecystokinin (CCK), secretin, and gastric inhibitory peptide appear to suppress gastric motility, at least in the dog. The roles of the various GI hormones are difficult to determine from available information, because many of the experimental results reported have been in response to administration of GI hormones at amounts far greater than those normally occurring.