Gastric Secretion
Ms. Priya Mathew
Assistant Professor
Department of Physiology
YNYSCH
LEARNING OBJECTIVES
The student will be able to: (MUST KNOW)
1. List the functions of stomach.
2. Outline the structure of gastric glands.
3. Understand the difference in the structure of resting and
activated parietal cell
4. List the composition and functions of gastric juice.
5. Describe the mechanism of HCl secretion
6. Describe regulation of gastric secretion in different phases.
FUNCTIONAL ANATOMY
Anatomically, stomach is divided into three major parts: fundus,
body and antrum. Esophagus opens into stomach through lower
esophageal sphincter (LES).
Initial portion of stomach close to gastroesophageal junction is
called cardia. The proximal part of stomach is called fundus, the
middle and major part of stomach is the body or corpus, and the
distal portion of the stomach is the antrum. Antrum opens into
the duodenum through pylorus which contains pyloric sphincter.
The capacity of the stomach depends on age, gender and eating
habit. On average, it is about 1.5 liter in adults, though it varies
from 1 to 4 liters.
The mucous membrane of stomach is thick and thrown into
large folds, called gastric rugae. These rugae are more prominent
in empty stomach.
The mucosal epithelium is formed by simple columnar epithelial
cells that secrete mucous and alkaline fluid.
These mucous and alkaline fluids protect gastric epithelium from
acidic content and mechanical injury. The mucosal surface of
stomach is studded with gastric pits (faveola) into which gastric
glands empty.
The gastric glands are situated deep in the mucosal infoldings
that open into the pits.
GASTRIC GLANDS
The mucosal lining of the stomach is a glandular mucosa that contains
surface mucous cells in the gastric pit and glands deep in the mucosal
infoldings.
There are three types of gastric glands:
1. CARDIAC GLANDS: Located below the lower esophageal sphincter and
contain mainly mucous secreting cells. They secrete mucous and
bicarbonate ions.
2. 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.
OXYNTIC GLAND
The acid secreting oxyntic gland is typically a tubular and straight gland. It
consists of neck, body and base. The cells in the neck are mainly mucous
secreting cell. The oxyntic cells are present mainly in the body of the gland.
Chief or peptic cells are present at the base.
CELL TYPES: Different cell types in the oxyntic glands are:
1. 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.
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.
Structure of Oxyntic Cells
Oxyntic cells or parietal cells are present in the body and neck of the oxyntic
glands. They secrete hydrochloric acid and intrinsic factor.
They have extensive tubulovesicular system and open canalicular system.
GASTRIC JUICE
VOLUME & pH: 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.
Composition of Gastric Juice
1. Water (99.5%)
2. Solids (0.5%)
Inorganic Constituents: Anions are Cl–, PO43–, SO42–, 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.
GASTRIC SECRETION
Mechanism of HCl Secretion
HCl is secreted from parietal cells that are located in the fundus and body of the stomach.
H+-K+ pump actively pumps H+ out of the cell into the gastric lumen.
In exchange for H+, the K+ enters the cell.
In the cytosol of parietal cell, H+ is derived from the breakdown of carbonic acid (H2CO3).
H2CO3 is formed by combination of CO2 and H2O in a reaction catalyzed by carbonic
anhydrase.
CO2 utilized for formation of H2CO3 is derived from intracellular metabolisms and plasma.
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. In the lumen,
Cl– combines with H+ to form HCl.
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.
Recycling of K+: K+ that enters the oxyntic cell by H+-K+ ATPase is transported back
into the gastric lumen, which is reutilized for further H+secretion (recycling of K+).
K+ entering the cell from interstitial fluid through basolateral membrane (by the
action of Na+-K+ pump located on basolateral membrane) is also secreted into the
lumen.
Thus, adequate K+ is available in the lumen for effective H+-K+ pump activity.
REGULATION OF GASTRIC
SECRETION
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.
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.
The vagal fibers that directly contact parietal cells are cholinergic and fibers
that contact G cells are noncholinergic (neurotransmitter is GRP).
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.
Experimental Design to Study Cephalic Phase
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.
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. 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.
Then, bilateral vagotomy is performed and the gastric juice is collected following
vagotomy for analysis.
Vagotomy abolishes gastric secretion during cephalic phase, which proves that
this phase is primarily vagally mediated
Gastric Phase
Starts when food enters the stomach.
The primary stimulus is the distension of the stomach.
Also, products of digestion like peptides and amino acids stimulate
gastric secretion.
The distension of the stomach elicits acid secretion by both local as well as
central reflexes.
The central reflex is mediated by vagus nerve 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.
Amino acid and peptides stimulate G cells to release gastrin.
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. However, the pouch experiment to study gastric secretion is not
performed now-a-days. This is mainly of academic and historical importance.
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.
Heidenhain pouch is a denervated pouch, which helps to study the influence of
neural factors on gastric secretion
Intestinal Phase
When chyme enters the intestine, intestinal phase of gastric secretion starts. This is
also called post-gastric phase. Initial part of intestinal phase is stimulatory to gastric
secretion, but later part is inhibitory.
Stimulation of Secretion
Distension of duodenum increases gastric acid secretion by activating vagovagal reflex.
The chemical composition of chyme, especially the products of protein digestion like
amino acids and peptide stimulate G and other endocrine cells in the duodenum and
upper jejunum to secrete entero-oxyntin, which in turn stimulates gastric acid
secretion
Inhibition of Secretion
Acidic chyme in the duodenum (decreased pH of duodenal content) inhibits gastric
secretion via ENTEROGASTRIC REFLEX.
Acid also stimulates release of secretin, which inhibits gastrin secretion from G
cells. Secretin also decreases the response of parietal cells to gastrin and
histamine.
Acid in the duodenum and hyperosmolality of duodenal content also secrete a
hormone called bulbogastrone that inhibits acid secretion from parietal cells of
the stomach.
Products of fat digestion especially fatty acids and triglycerides stimulate
secretion of GIP and CCK from upper part of small intestine. These hormones
inhibit secretion of acid from parietal cells.
Thus, the net effect of intestinal phase is the inhibition of gastric secretion.
Hence, intestinal phase accounts for about 10% of gastric secretion.
GASTRIC FUNCTION TESTS
They include:
Examination of gastric contents
Test for gastric acid secretion
Tests for pepsin, mucous, intrinsic factor
Tests for gastrin
Visualization of the interior of stomach
Tests for gastric motility and electrical activities (gastrography)
Obtaining biopsy from the suspected tissue
APPLIED ASPECTS
Gastritis
Any clinical condition with upper abdominal discomfort like indigestion or dyspepsia. The
condition is of great importance due to its relationship with peptic ulcer and gastric cancer.
Broadly, gastritis is of 2 types: acute and chronic.
Etiopathogenesis
Diet and personal habits:
Infections
Drugs
Chemical and physical agents
Severe stress
Chronic gastritis, if untreated leads to peptic ulcer.
Peptic Ulcers
Peptic ulcer means ulcer in the stomach (gastric ulcer) or duodenum (duodenal
ulcer).
Pathophysiology: Peptic ulcer is caused either by decreased mucosal defense, or by
hypersecretion of acid or infection.
A. Diminished effectiveness of Mucosal Barrier
The defense barrier of the stomach is the mucous coat on the gastric epithelium.
This is called mucosal defense barrier.
The mucus is secreted by mucous cells. Mucus is a viscous gel that contains
mucin, phospholipid, electrolytes (mainly HCO3–) and water.
The mucous gel layer is about 0.2 mm thick and effectively separates the
bicarbonate rich secretion of epithelial cells from the acidic content of the
stomach.
This allows the pH of the epithelial cells to remain alkaline. It protects mucosal
epithelium from injury caused by acidic chyme.
