Salivation
The process of digestion starts in the mouth with mastication, in which the physical breakdown of food is combined with saliva. Salivation occurs as saliva is produced by the parotid, submandibular and sublingual glands, and saliva lubricates the mouth, aids dental hygiene, adds fluid to the food and initiates the breakdown of starches by addition of amylase. Acinar cells secrete amylase and electrolytes with similar tonicity to plasma, and striated and excitatory ducts modify secretions. A healthy human produces about 1–1.5 L of saliva per day.
Control of salivation (Figure 42.1)
This process is under autonomic control with parasympathetic nerves releasing acetylcholine (ACh) to act at muscarinic receptors to increase the production of saliva and increase blood flow to promote fluid movement. Parasympathetic nerves also release vasoactive intestinal polypeptide (VIP), which causes vasodilatation to enhance saliva secretion. Parasympathetic control makes the saliva watery (hypotonic relative to plasma), while sympathetic control increases its viscosity. Drugs with antimuscarinic side effects may block the production of saliva as a side effect, leading to a dry mouth.
Gastric physiology
The food is then swallowed, which is largely a reflex action (controlled via the swallowing centre in the medulla and lower pons), and the bolus of food then passes down the oesophagus via peristalsis, through the lower oesophageal sphincter and into the stomach. Food is retained in the stomach for several hours, during which time the gastric mucosa releases acid (pH of the gastric contents is pH1–1.5) and proteolytic enzymes to initiate the breakdown of proteins. Chief cells of gastric mucosa release pepsinogens and the acid environment activates these to form pepsins. This is also an autocatalytic process as the newly formed pepsin activates further pepsinogens, which are endopeptidases and so act within peptide chain. The acidic environment is also the optimum pH for pepsin activity.
Gastric acid secretion (Figures 42.2, 42.3 and 42.4)
The production of gastric acid is a tightly regulated process. Parietal cells of the gastric mucosa contain H+/K+ ATPases (proton pumps) on their lumenal surfaces and these antiport H+ out of the cell in exchange for K+. Gastric acid secretion is under cephalic control (central control stimulated by the presence of food in the mouth and chewing), which involves direct parasympathetic vagal stimulation and indirect parasympathetic control via the release of histamine from enterochromaffin (ECF)-like cells. For direct control, ACh acts at muscarinic M3 receptors, which couple via increasing intracellular calcium to activate the proton pump. Histamine released from the ECF-like cells acts on histamine H2 receptors to increase cAMP, which also activates the proton pump via phosphorylation. The final stimulatory pathway is via the hormone gastrin. Gastrin is released by G-cells of the antrum and leads to the gastric phase. The release of gastrin is stimulated by the presence of the food in the stomach, passes via the bloodstream to act on the stomach and the gastrin acts at cholesytokinin CCK2 receptors to stimulate histamine release from the ECF-like cells and also directly on parietal CCK2 receptors to cause calcium-dependent proton pump activation. The final phase of control is the intestinal phase, in which protein digestion products stimulate the release of gastrin from G-cells.
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