Gastrointestinal Control

 

Control of GI Function

GI function is controlled by neural and chemical regulation. There are three phases of GI regulation - cephalic, gastric, and intestinal.

Neural Regulation

The extrinsic, or autonomic, system consists of the parasympathetic system, represented by the vagus and pelvic splanchnic nerves. The sympathetic system originates from the celiac, superior mesenteric, and inferior mesenteric ganglia.

The gut also contains the enteric nervous system, a discrete web of 100 million neurons that can control gut function without extrinsic control. It consists of the myenteric plexus, located between longitudinal and circular muscle layers, and the submucosal plexus.

Reflexes mediate motility, secretions, hormone release, and vasculature. Long reflexes go from gut mechano- and chemoreceptors along the vagus to the brain, and back. Short reflexes are mediated exclusively by the enteric nervous system.

Short reflexes include the gastroenteric, enterogastric, and gastrocolic reflexes.

Stomach Pacemaker Cells

Gut smooth muscle has a basic electrical rhythm, where once every 3-5 minutes there is a change in resting potential in pacemakers cells in the stomach.

Normally these changes do not reach the threshold for contraction. However, with stimulation from the vagus or hormones such as gastrin, the threshold is crossed and contraction occurs.

Contraction strength increases with stimuli strength, but there is no change in contraction frequency.

Chemical Regulation

The GI system is also regulated by both paracrine and endocrine hormones. Most of these originate from within the GI system.

 

GI hormones are expressed at various points during feeding to regulate digestion and GI motility.

Most GI hormones are polypeptides and therefore have a short half-life.

 

GI Hormones
Hormone Source Stimulus Major Actions
Gastrin G cells in antrum and duodenum ACh, antral distension, digested protein acid secretion, mucosal growth, antral motility
Cholecystokinin (CCK) I cells in SI fat, digested protein pancreatic enzyme and bile secretion, relaxation of Sphincter of Oddi, decreased gastric emptying
Secretin S cells in duodenum pH < 4.5 pancreatic and bile bicarbonate secretion, decreased acid secretion
Glucose-dependent Insulinotropic peptide (GIP) K cells in duodenum and jejunum glucose, fat insulin secretion
motilin endocrine cells in duodenum, jejunum neural stimulation migrating motility complex

GI Paracrine Regulators
Molecule Source Stimulus Major Actions
somatostatin D cells in stomach and SI ph < 3, digested fat decreased gastrin and gastric acid release
histamine gastric mast cells ACh, gastrin potentiates parietal cells

 

Hormone Deregulation

Zollinger-Ellis Syndrome is a gastrin secreting tumour. As gastrin causes mucosal growth, the stomach of patients can become quite overgrown.