Gastric Secretions

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Chief of Pepsi cola = Chief cells secrete PEPSInogen

Parietal cells: secrete HCl, Ca, Na, Mg and

intrinsic factor

Chief cells: secrete pepsinogen

Surface mucosal cells: secrete mucus and

bicarbonate

Gastric

secretions

A working knowledge of gastric secretions is important

for surgery because peptic ulcers are common, surgeons frequently prescribe

anti secretory drugs and because there are still patients around who will have

undergone acid lowering procedures (Vagotomy) in the past.

Gastric acid

Is produced by the parietal cells in the stomach

pH of gastric acid is around 2 with acidity being

maintained by the H+/K+ ATP

ase pump. As part of the process bicarbonate ions will be secreted into

the surrounding vessels.

Sodium and chloride ions are actively secreted

from the parietal cell into the canaliculus. This sets up a negative

potential across the membrane and as a result sodium and potassium ions

diffuse across into the canaliculus.

Carbonic anhydrase forms carbonic acid which

dissociates and the hydrogen ions formed by dissociation leave the cell

via the H+/K+ antiporter pump. At the same time sodium

ions are actively absorbed. This leaves hydrogen and chloride ions in the

canaliculus these mix and are secreted into the lumen of the oxyntic

gland.

This is illustrated diagrammatically below:

Image

sourced from Wikipedia

Phases of gastric acid secretion

There are 3 phases of gastric secretion:

1. Cephalic phase (smell / taste of food)

30% acid produced

Vagal cholinergic stimulation causing secretion

of HCL and gastrin release from G cells

2. Gastric phase (distension of stomach )

60% acid produced

Stomach distension/low H+/peptides causes Gastrin release

3. Intestinal phase (food in duodenum)

10% acid produced

High acidity/distension/hypertonic solutions in

the duodenum inhibits gastric acid secretion via enterogastrones (CCK,

secretin) and neural reflexes.

Regulation of gastric acid production

Factors increasing production include:

Vagal nerve stimulation

Gastrin release

Histamine release (indirectly following gastrin

release) from enterchromaffin like cells

Factors decreasing production include:

Somatostatin (inhibits histamine release)

Cholecystokinin

Secretin

The diagram below illustrates some of the factors involved in regulating

gastric acid secretion and the relevant associated pharmacology

Image

sourced from Wikipedia

Below is a brief summary of the major hormones involved in food digestion:

Source

Stimulus

Actions

Gastrin

G cells in antrum of the stomach

Distension of stomach, extrinsic nerves

Inhibited by: low antral pH, somatostatin

Increase HCL, pepsinogen and IF secretion, increases gastric motility,

trophic effect on gastric mucosa

CCK

I cells in upper small intestine

Partially digested proteins and triglycerides

Increases secretion of enzyme-rich fluid from pancreas, contraction of

gallbladder and relaxation of sphincter of Oddi, decreases gastric emptying,

trophic effect on pancreatic acinar cells, induces satiety

Secretin

S cells in upper small intestine

Acidic chyme, fatty acids

Increases secretion of bicarbonate-rich fluid from pancreas and

hepatic duct cells, decreases gastric acid secretion, trophic effect on

pancreatic acinar cells

VIP

Small intestine, pancreas

Neural

Stimulates secretion by pancreas and intestines, inhibits acid and

pepsinogen secretion

Somatostatin

D cells in the pancreas and stomach

Fat, bile salts and glucose in the intestinal lumen

Decreases acid and pepsin secretion, decreases gastrin secretion,

decreases pancreatic enzyme secretion, decreases insulin and glucagon

secretion

inhibits trophic effects of gastrin, stimulates gastric mucous production

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