The stomach acts as a reservoir for food, releasing the gastric contents into the duodenum at a steady rate. Relaxation of the LOS and arrival of food in the stomach is followed by a receptive relaxation of the fundus and body of the stomach. This is mediated by a vagal reflex, which inhibits the smooth muscle tone in this area (via the vagal inhibitory fibres with release of VIP and nitric oxide). The vagal inhibitory fibres cause relaxation by inducing hyperpolarization. The average adult produces 2–3 L of gastric juice every 24 hours. Gastric juice contains mucus, digestive enzymes (pepsinogen and lipase), HCl and intrinsic factor.
Resting juice is an isotonic juice secreted by the surface cells. It is similar to plasma, but it has an alkaline pH of 7.7 and a higher concentration of HCO3¯.
Mucus is secreted by goblet cells of the surface epithelium and mucus neck cells, especially in the pyloric antrum. The alkaline mucus of the stomach is a thick, sticky mucopolysaccharide. It is secreted with HCO3¯ ions, which are exchanged for Cl¯ ions by the epithelial cells. It plays an important role in the protection of the stomach against its acid contents. Mucus forms a water-insoluble gel that adheres to the surface of the stomach lumen. It reduces the flow of H+ ions and acts as a barrier to pepsin. Although pepsin can degrade mucus, the HCO3¯ secretions increase the pH and make the enzyme less active.
Pepsin is secreted from the chief cells in the gastric pits in the form of its precursor, pepsinogen. HCl activates pepsinogen by cleaving off nine amino acid residues to form pepsin. Pepsin is a proteolytic enzyme that acts on proteins and polypeptides, by hydrolysing internal peptide bonds.
Gastric lipase is an enzyme that acts on triglycerides to produce fatty acids and glycerol. It is useful in facilitating subsequent hydrolysis by pancreatic lipases, but it is of little physiological importance except in pancreatic insufficiency.
Intrinsic factor (IF) is made in the parietal cells of the stomach; it is a glycoprotein vital for the absorption of vitamin B12 via receptors for IF-B12 in the terminal ileum. Without intrinsic factor, vitamin B12 is digested in the intestine and not absorbed. R-proteins in the saliva and stomach protect vitamin B12 until it is absorbed. Upon absorption, it is bound to transcobalamin II, which serves to transport it in plasma. Most diets contain excess vitamin B12 and stores are built up in the liver. These stores last for 2–3 years; thus, it takes considerable time for a dietary deficiency to produce symptoms.
HCl is produced by the parietal (oxyntic) cells. The concentration of HCl depends on:
- The rate of HCl secretion
- The amount of buffering provided by the resting juice, ingested food and drink and the alkaline secretion of the pyloric glands, duodenum, pancreas and bile
- Gastric motility
- The rate of gastric emptying
- The amount of diffusion back into the mucosa
The pH of the contents of the stomach after feeding is normally about 2–3. Gastric HCl provides a defence mechanism that is non-specific in killing ingested microorganisms. It also aids protein digestion (by enabling the activation of pepsin from pepsinogen) and stimulates the flow of bile and pancreatic juice. Secretion is inhibited by vagotomy (which removes acetylcholine stimulation) and pharmacologically, the latter of which is covered in the next section.