3. Gastric gland
There are three types of gastric glands:
1. The cardiac glands: Located below the lower esophageal sphincter and contain mainly
mucous secreting cells. They secrete mucous and bicarbonate ions.
2. The oxyntic glands: Located in the fundus and body of the stomach and contain
mainly the oxyntic cells.
3. Pyloric glands: Present in the pyloric-antral region and consist mainly of mucous neck
cells that secrete mucous and G cells that secrete gastrin.
4. Oxyntic Gland
• The oxyntic cells are present mainly in the body of the gland. Chief or peptic cells are
present at the base.
• Mucous cells: They are present in the neck region of the gland. The mucous and
bicarbonate ions secreted by them protect the stomach epithelium from acidic gastric
secretion.
• 2. Oxyntic or Parietal cells: Oxyntic cells are present mainly in the body part of the
gland. They secrete hydrochloric acid and intrinsic factor.
• 3. Chief or peptic cells: Chief cells are present towards the base of the gland. They
secrete pepsinogen.
• 4. Endocrine cells: The endocrine cells are also called enterochromaffin cells. The
major endocrine cells in oxyntic glands are enterochromaffin-like cells (ECL) or mast-
like cells that secrete histamine. There are also other endocrine cells that secrete
somatostatin, VIP, glucagon, and enkephalin. G cells are present in antral region that
secrete gastrin. Antrum also contains D cells that secrete somatostatin.
6. Gastric juice
• The amount of gastric secretion per day varies from 1 to 2.5 liters.
• The gastric juice is highly acidic; having pH 0.7–4.
• 1. Water (99.5% 2. Solids (0.5%)
• Solids contain inorganic and organic substances.
• Inorganic constituents: Anions are Cl–, PO4 3–, SO4 2–, and HCO3 –; and cations are H+, Na+, K+, Ca2+, and
Mg2+.
• Organic constituents: Pepsinogen, intrinsic factor, mucin, rennin, gastric lipase, gelatinase, carbonic
anhydrase, and lysozyme.
• Functions of Constituents
• Normal concentration of HCl is 40–60 mEq/L. The maximum concentration can increase upto 150 mEq/L:
• 1. Pepsinogen is secreted from the peptic cells. There are two types of pepsinogens:
• −− Type-I pepsinogen is found in chief cells in fundus and body.
• −− Type-II pepsinogen is found in the chief cell throughout the stomach.
7. • Pepsinogen is converted into pepsin by HCl.
• Pepsin is a proteolytic enzyme that breaks down protein molecules into
peptones.
• Pepsin acts best at pH of 2–4.
• 3. The mucin secreted by mucous cells is of two types: the insoluble
mucin, and the soluble mucin.
• Mucin forms a protective layer on the gastric epithelium. It retains
bicarbonate and has alkaline pH. Thus, it protects the stomach from acid
peptic digestion, as it buffers HCl.
• 4. Intrinsic factor helps in vitamin B12 absorption from terminal ileum.
8. Hcl secretion
• HCl is secreted from parietal cells that are located in the fundus and body of the stomach.
• H+ secretion -H+–K+ ATPases in apical membrane of the parietal cells
• HCO3 – formed by break down of H2CO3 is exchanged for Cl– on the basolateral membrane of the cell by
HCO3 –-Cl– exchanger.
• The Cl– that enters parietal cell is transported into the gastric lumen.
• The HCO3 – enters blood stream from the interstitial fluid.
• Thus, for each H+ secreted into the gastric lumen, one HCO3 –is reabsorbed into the plasma. Therefore, with
increase in the rate of HCl secretion, HCO3 – level increases in the blood.
• Following a meal that stimulates gastric acid secretion, pH of blood increases. As blood becomes alkaline,
the urine becomes alkaline.
• This is called post-prandial alkaline tide.
13. Regulation of Gastric Secretion
• Gastric secretion is regulated by neural and humoral mechanisms.
• The mechanism of regulation depends on the phase of gastric acid secretion.
• The neural mechanisms are autonomic influences, short and long GI reflexes,
and central influences mediated by vagus nerve.
• The hormonal mechanisms regulating gastric
• Gastric secretion occurs in three phases (cephalic, gastric and intestinal) and the
mechanisms regulating secretion are different for each phase of secretion.
14. Cephalic phase
• The cephalic phase of gastric secretion is elicited by smell, sight, thought, taste and chewing of food. This is
called cephalic phase as impulses to increase acid secretion originate mainly in the brain:
• 1. The sensory stimuli activate dorsal motor nucleus of vagus in the medulla. Therefore, cephalic phase of
gastric secretion is entirely mediated by vagus nerve and the fibers are both cholinergic and noncholinergic
• 2. The vagal fibers that directly contact parietal cells are cholinergic and fibers that contact G cells are
noncholinergic (neurotransmitter is GRP).
• 3. As noncholinergic effects are stronger than cholinergic effects, atropine can not effectively prevent vagally
mediated acid secretion. Therefore, atropine is not prescribed in the management of peptic ulcer.
• The gastric juice secreted in the cephalic phase occurs before food reaches the stomach. Therefore, this is
also called pregastric phase. This phase accounts for 40–50% of total gastric secretion
15. Experimental evidence
• The usual experimental design to assess the integrity of the
cephalic phase is the sham feeding. In this procedure, a dog is
taken as the experimental animal:
• 1. A fistula is made in the esophagus of the dog; so that when
animal eats the food comes out of the neck through the fistula
(food is not allowed to reach stomach).
• Simultaneously, the gastric juice is collected from the stomach by
placing a cannula into it
• Gastric juice obtained during the cephalic phase is analyzed for
volume and composition.
• 2. Then, bilateral vagotomy is performed and the gastric juice is
collected following vagotomy for analysis.
• 3. Vagotomy abolishes gastric secretion during cephalic phase,
which proves that this phase is primarily vagally mediated.
16. Gastric phase
• The gastric phase of gastric secretion starts when food enters the stomach:
• 1. The primary stimulus for secretion in this phase is the distension of the stomach.
• 2. Also, products of digestion like peptides and amino acids produced by pepsin action
that breaks proteins stimulate gastric secretion.
• 3. The distension of the stomach elicits acid secretion by both local as well as central
reflexes. The central reflex is mediated by vagus nerve (vagovagal reflex), and is both
cholinergic and noncholinergic. The local reflex releases acetylcholine that directly
stimulates parietal cell. Distension of stomach per se also increases gastrin release from
the antral G cells that in turn increases HCl secretion.
• 4. Amino acid and peptides stimulate G cells to release gastrin.
• 5. Therefore, mechanisms of acid secretion in the gastric phase are mechanical, neural,
and chemical.
• 6. Gastric phase accounts for 50–60% of gastric secretion.
17. • HCl secretion in this phase is decreased by the acidic pH of the chyme bathing in the gastric mucosa. When
pH of gastric content becomes less than 2, HCl secretion is effectively reduced. This is called autoregulation
of gastric acid secretion
• HCl inhibits both G cells and parietal cells.
18. • Experimental Designs to Study Gastric
Phase
• Gastric phase of gastric secretion is studied by
making five different types of pouches: Pavlov
pouch, Heidenhain pouch, Bickel pouch, Farrell
pouch and Ivy pouch.
• 1. Pavlov pouch is a small pouch separated
from the main body of the stomach by a double
layer of mucous membrane.
• This gastric pouch of mucous membrane has
intact nerve and blood supply.
• Therefore, it helps to study both neural and
chemical factors of gastric acid secretion.
20. Heidenhain pouch is a
denervated pouch, which helps
to study the influence of neural
factors on gastric secretion.
21. Heidenhain’s pouch experiment to demonstrate existence of some blood-borne mechanism regulating
gastric
secretion.
• 2. Heidenhain pouch is a denervated pouch, which helps to
• study the influence of neural factors on gastric secretion
• Heidenhain’s pouch is modified Pavlov’s pouch which is separated in such a way from the antral
part of stomach that it is denervated but with intact blood supply
• Distension of the denervated pouch (with intact blood supply) induces gastric secretion. Occurrence
of gastric secretion in a denervated pouch of stomach demonstrates that there exists some blood-
borne mechanism which also regulates gastric secretion.
• Intravenous injection of gastrin is followed after 5 min by secretion of gastric juice from the
denervated Heidenhain’s pouch.
• This demonstrates that bloodborne mechanism is mediated by a gastrin hormone released from the
antral mucosa.
