Gastric secretions and functions

• the stimulation of parietal cells will result in secretory canaliculus • H+ pumps will be incorporated into the canaliculus membrane • this will pump H+ into the lumen and K+ into the cell • Cl- will leave the cell via a Cl- channel and K+/Cl- symporter will also allow K+ to leave the cell • the ionisation of water in the cell will produce H+ and OH- • OH- is removed from the cell in the form of bicarbonate • Cl- will enter the cell in exchange for bicarbonate • H+ and Cl- will combine to form HCl in the lumen • carbonic anhydrase is important in driving H+ production

• basal secretion of Na+ comes from non parietal cells • stimulated secretion of H+ and Cl- comes from parietal cells • it is isotonic • although the concentration of ions changes the osmolarity of gastric secretions doesn’t change

1) cephalic phase - when the food hasn’t yet entered the GI tract and it is currently in the mouth 2) gastric phase - when the food has entered the body and into the stomach 3) intestinal phase - when food leaves the stomach and enters the small intestine

Integrated control is via : - sensory receptors - nervous pathways - hormones e.g. gastrin - paracrine agents e.g. histamine and somatostatin

• 30% of gastric secretions are stimulated in this phase 1) sight, smell and the taste of food will cause vagal stimulation 2) this will lead to secretion of acetylcholine by nerve endings 3) this will lead to secretion of gastrin by G cells in the stomach 4) this stimulates parietal cells to secrete HCl and chief cells to secrete pepsinogen 5) HCl will lower the pH of the stomach leading to inhibition of gastric secretion 6) pepsinogen will stimulate peptides in the stomach which stimulates gastric secretions

• 60% of gastric secretions are stimulated in this phase 1) distension of the stomach stimulates mechanoreceptors, chemoreceptors and osmoreceptors 2) this will stimulate vago-vagal and local reflexes resulting in the secretion of acetylcholine by nerve endings 3) the remainder of this phase is the same as the cephalic phase

• part of the parasympathetic nervous system • have cholinergic nerve fibres • binds Acetylcholine

They activate the same internal pathway as acetylcholine

they increase the effects of gastrin

• gastrin binds to CCK2 receptors and acetylcholine binds to muscarinic receptors • this causes the release of calcium ions from the endoplasmic reticulum • these stimulate the H+/K+ pump • histamine binds to its receptor • this produces protein kinase A • this leads to phosphorylation of certain parietal cell proteins which include H+/K+ pump • somatostatin and prostaglandins bind to their receptors • this inhibits the formation of cAMP • they have inhibitory effects in terms of releasing H+ ions

nervous = - enteric nervous system involved in short reflexes - ANS involved in long reflexes hormones = - gastrin from G cells in the stomach - secretin from S cells in the small intestine

• 5% of gastric secretions stimulated in this phase 1) protein digestion products in the duodenum stimulate G cells in the small intestine and secretion of enterogastrone hormones 2) G cells in the small intestine lead to stimulation of parietal and chief cells 3) enterogastrone hormones inhibit G cells of the stomach and inhibit parietal cells and chief cells

• gastric secretion is inhibited at low pH as D cells release somatostatin • gastric secretion is inhibited by the inhibitory intestinal phase through the production of enterogastrones as they inhibit parietal cells

• frequency of contraction is constant and the basal electrical rhythm of the stomach can’t be changed • force of contraction is variable and is controlled by neural and hormonal input • during a peristaltic wave the lower sphincter is closed and so the antrum will churn the trapped material • the bolus will be pushed back into the proximal stomach causing the sphincter to open a little bit and some chyme will leave and enter the duodenum (this is called retropulsion)

• if the conditions of the small intestine are not favourable this will stimulate neural receptors and the secretion of enterogastrones • neural receptors activate short and long reflexes decreasing gastric emptying • enterogastrones increase plasma enterogastrones and decrease gastric emptying

• muscarinic cholinergic receptors • gastrin receptors • histamine receptors