Control of gastric secretion

CONTROL OF GASTRIC SECRETION
  • In man and horse, the secretion of gastric juice is continuous but it is intermittent in dogs and cats.
  • The rate of secretion increases during feed intake.
  • The secretions of gastric glands are regulated by nervous and chemical mechanisms.
  • The gastric secretion takes place in three phases 

Cephalic phase

  • Stimulation of sensory endings in mouth and pharynx or psychic/conditioned reflex due to the impulses originating from the smell, sight of food sensation provoke the cephalic phase of secretion. It contributes about 45% of gastric secretion. The extent of psychic secretion is well developed in dogs and also present in pigs.

Gastric phase

  • Entry of food into the stomach causes copious secretion of gastric juice. This contributes about 45% of the gastric secretory response.
  • Basically two principle stimuli are responsible for gastric phase
    • Mechanical stimuli
    • Humoral /hormonal stimuli
  • Mechanical stimulation
    • Stimulation of intrinsic nerve system
    • Vago-vagal reflex from fundic area
      • Contact of food bolus with the receptors of stomach mucous membrane and the distension of the stomach causes the releases of acetylcholine. Both “G” cells and parietal cells of the gastric glands are stimulated by acetylcholine results in increased secretion of gastrin and HCl respectively.

Hormonal stimulation

  • Major portion of gastrin, a gut hormone is produced by the “G” cells of the pyloric glands. Small amount of gastrin is also released from the fundus, duodenum and small intestine. Vagal stimulation during anticipation of eating and distension of stomach stimulates gastrin release and HCl secretion. 

  • Histamine present in the gastric mucosa is also a powerful stimulator of gastric acid secretion.Histamine is secreted by enterochromaffin-like cells (ECL)  in parietal mucosa. Acetylcholine produced by parasympathetic nerve endings also stimulate HCl secretion by the parietal cells. Vagus conditioned the parietal cells and potentiates the action of gastrin on HCl secretion. Gastrin stimulates the gastric juice with high HCl content and low pepsin activity. The pepsin release is not hormonally stimulated, but its secretion is enhanced by vagal stimulation.

Intestinal phase

  • Accumulation of food in the intestine excite gastric secretion by humoral mechanism due to entry intestinal gastrin and cholecystokinin (CCK) from duodenum into gastric gland through blood stream. This phase contributes about 10% of the gastric secretion.
  • Secretion and functions of mucus
    • The gastric mucus is derived from cardiac and pyloric glands, neck chief cells of fundic glands and surface epithelium of stomach. Mucus secretion is independent of secretion of water, HCl and enzymes. Vagus controls the mucus secretion. Mucous functions as a lubricant and protects the to gastric mucous membrane of stomach wall against the highly HCl content.
  • Inhibition of gastric secretion
    • Gastric secretion may be inhibited by higher nerve centers via  smell or sight of unappetizing food. The autonomic nervous system is involved in marked inhibition of gastric secretion during pain, anger and other emotional states.
    • Accumulation of acid (< pH 2.5) in the stomach inhibits further HCl production by inhibiting gastrin release from pylorus.
    • Entry of fat, sugar, or high acid contents into the duodenum, causes the release of gastric inhibitory polypeptide (GIP), from the duodenum. It is transported to stomach via blood stream and inhibits gastric secretion. Secretin and CCK secretions from the duodenum are also involved in the inhibition of gastric secretion, when acid contents of stomach enter the duodenum.
Last modified: Thursday, 15 September 2011, 4:47 AM