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Composition of the

gastric juice
About 99% gastric juice mass is water, while
the remaining consists of both organic and
inorganic matter.
The organic matter consists of
Pepsinogens[precursors Of Pepsins]
Gastric Lipase
Intrinsic factor
A trace of lactic acid
The most important inorganic constituent is
Other inorganic constituents are
1.3 to 2.6
Secretion /day
Two to three liters
1. HCI:
(i) lt activates pepsinogen to pepsin.
(ii) It lowers the pH of the gastric juice so that
pepsin can have a favorable pH for digestion of
(iii) lt has an antiseptic action which prevents
the growth of microorganisms in the stomach.
When gastric juice is low in HCL
(hypochlorhydria) or when HCI is totally absent
(achlorhydria), there occurs microbial growth
in the stomach as shown by an increased lactic
(iv) It helps in the absorption of iron as it helps
in the release of iron from its bound form in
food ; moreover, it has a role in converting
ferric to ferrous form which is easily absorbed.
(v) When the gastric contents enter the
duodenum, the HCl contained in them
stimulates the release of a hormone namely
secretin into the blood stream.
HCl increase:
HCl decrease:
Prostaglandin (PG)
2. Pepsin:
lt is secreted in the inactive zymogen form
called pepsinogen which is initially activated to
pepsin by the HCl present in the gastric juice;
activation occurs rapidly at a pH below 2.

Once some pepsin has been formed, it can

itself activate more of pepsinogen by what is
called- autocatalytic process.
Pepsin is a powerful proteinase and exerts the
following actions:

(i) lt converts proteins to smaller fragments, i.e.

polypeptides by hydrolyzing specific peptide

(ii) lt curdles milk. This occurs due to the

conversion of the milk protein casein into
paracasein. by a partial hydrolysis. Paracasein
combines with Ca2+ ions to form calcium
3. Gastric
Its activity lipase:
is confined to the stomach as it is
destroyed by trypsin.
lt is much more active against fats containing
short and medium chain fatty acids, e.gr milk
It is stable in acid medium.
4. Mucins:
These are carbohydrate-containing proteins
that are present in the mucus, and act as
lubricating agents by forming a slippery layer
over the mucosa of the stomach.
This layer of mucin also acts as a barrier to the
action of gastric juice on stomach wall and
thus helps in preventing the digestion of the
stomach itself; moreover, mucin has an anti-
pepsin activity and also has a buffering action
against HCL.
5. Intrinsic factor:
This factor is glycoprotein in nature and is
required for the active absorption of vitamin B
12 from the ileum.
Its lack results in vitamin B 12 deficiency and
produces pernicious anemia.
The formation of the intrinsic factor is the
only function of the stomach that is essential
for life.
Role of gastric juice
The hypotonicity of the gastric juice helps in
decreasing the tonicity of the hypertonicy
ingested food towards isotonicity with plasma.

ln patients whose stomach has been

removed, this function is lost and the entry of
hyperosmotic food into the small intestine
results in severe symptoms collectively
termed the dumping syndromes
Mechanism of HCl
The secretion of HCl is an active process
(Proton Pump)
needing ATP.
The parietal cell has a basolaterel portion and
an apical portion.
There is an intracellular canaliculus into which
ions like H+, Cl- and K+ and water make
entry; from here HCl and water are pomed
into the glandular lumen and thereafter into
the gastric lumen.
1. The enzyme carbonic anhydrase catalyzes
the reaction CO2 + H2O > H2CO3.
2. H2CO3 splits into H+ and HCO3. The
importance of this enzyme action in HCl
production is shown by the fact that
administration of its inhibitor acetazolamide,
decreases HCI formation.
3. The H+ ion is actively secreted into the
canaliculus of the parietal cell by H+ K+
ATPase also called the gastric proton pump.
This enzyme is inhibited by omeprazole which
4. The intracellular HCO3 is exchanged across
the basolateral membrane for extracellular Cl-
by the HCO3-/Cl- exchanger.
As Cl- concentration within the cell increases,
these ions are driven across the apical
membrane into the canaliculus, where along
with H+ they form HCl. The HCO3- enters the
interstitial fluid from where it passes on into
the blood.
lt is obvious that for each H+ secreted into the
gastric juice, one HCO3- enters the blood.

5. The intracellular K+ is kept at high level by

Na+K+ ATPase at the basolateral membrane.
Potassium ions move into the lumen of the
canaliculus and are used to drive H+K+
ATPase. Some K+ ions also diffuse into the
intracellular canaliculus.
The overall reaction can be summarized by
the equation,
CO2+ H20 + Cl- --------> HCl + HCO3-
Regulation of the
I. Basal or resting secretion:
Secretion of Gastric
. Basal secretion of HCI is more during night
and is least in the morning.
This can be divided into three phases which are
termed cephalic, gastric and intestinal
1. Cephalic or neural phase:
. This results from the stimulation of gastric
secretion produced by sight, smell, taste or
even thought of food.
2. Gastric phase:
This phase is seen when food enters the
stomach and stimulates the secretion of the
Distension by the stomach stimulates HCI
secretion by stimulating stretch receptors in
the wall and mucosa of the stomach.
3. Intestinal phase:
The intestinal influences on gastric secretion
are exerted through reflex and hormonal
feedback mechanisms.
The hormone through which this secretion is
Stimulants of Gastric
HCI Secretion
1. Parasympathetic
Vagal stimulation produces its effects by
releasing acetylcholine as well as-by releasing
gastrin and by decreasing release of
Cholinergic drugs, e.g.
pilocarpine are strong stimulants of gastric
2. Histamine:
It is a very powerful stimulant of parietal cells
and therefore the juice produced is rich in HCl.
Conditions in which histamine is liberated in
the body such as burns lead to a greater
secretion of the gastric HCI; this explains the
occurrence of peptic ulcers as a complication
of extensive burns (Curlings ulcers).
An analog of histamine, histalog, stimulates
gastric secretion, but does not produce the
undesirable side effects seen with histamine;
it is used for testing the gastric secretory
3. Gastrin:
its role has been already described. Gatrin
release from the G cells is increased by vagal
stimulation through release of gastrin
releasing peptide.
Gastrin acts through gastrin receptors of the
parietal cells but its main action is via
stimulating the release of histamine from the
enterochromaffin-like (ECL) cells.
A commercially available preparation is
pentagastrin which consists of the terminal
tetrapeptide part of the natural gastrin and in
addition contains a derivative of -alanine.
4: Ca2+ ions: These ions increase gastric
HCl Secretion. Peptic ulcer may occur in if
hypercalcemia states, e.g.
5. Caffeine: It is present in tea, coffee and
cola beverages.
6. Alcohol: It stimulates the secretion of a
juice rich in HCl by a direct action of the
gastric glands.
7. Nicotine: In small doses it stimulates
gastric glands.
8. Proteins: Food rich in proteins increases the
liberation of gastrin, whose effects have already
been described.
9. Food flavors: These include chillies,
condiments, etc. These act by adding it flavor to
the food which stimulates, the cephalic phase of
gastric secretion.
10. Alkalies: NaHCO3 in small doses increases
HCI secretion because alkaline pH in the pyloric
antrum stimulates the release of gastrin.
11. Psychological
Chronic anger, resentment and chronic
anxiety and fear increase the secretion of
gastric juice which is rich in HCl.
Peptic ulceration may be seen when a person
is faced with excessive stress (stress ulcers).
12. Medication:
Drugs that inhibit prostaglandin formation,
e.g. non- steroid anti-inflammatory drugs
(NSAID) that include acetylsalicylic acid
(aspirin) and many commonly used "pain-
killers" increase gastric acidity.
This is because prostaglandin decreases
gastric acidity.
13. Hormones:

By producing hypoglycemia insulin increases

secretion rich HCl through vagal center in the
brain; Glucocorticoids when given in large doses
over a long time also increase gastric acidity;
the effect is probably due to interference with
formation of antibodies against H. pylori.