The stomach secretes about 2 L of HCl per day. The concentration of H+ in the lumen of stomach may reach >150 mM, which is 1 to 3 million times greater than the concentration in the blood. This requires an efficient production mechanism to generate large number of hydrogen ions. The origin of the hydrogen ions is CO2 in parietal cells.
Primary H+/K+ ATPases in the luminal membrane of the parietal cells pump these hydrogen ions into the lumen of the stomach. H+ is secreted into the lumen, HCO3- is secreted on the opposite side of the cell into the blood in exchange for Cl- . Removal of the end products of this reaction enhances forward rate of reaction. In this way, production and secretion of H+ are coupled. Increased acid secretion results from the transfer of H+/K+ ATPases proteins from the membranes of intracellular vesicles to the plasma membrane by fusion of these vesicles with the membrane, thereby increasing the number of pump proteins in plasma membrane.
Four chemical messengers regulate the insertion of H+/K+ ATPases into the plasma membrane and therefore acid secretion : gastrin, acetylcholine, histamine and somatostatin. Somatostatin inhibits acid secretion, where other three stimulate secretion.
Cephalic and gastric phase also control secretion of HCl. During Cephalic phase, increased activity of efferent parasympathetic neural input to the stomach's enteric nervous system results in the release of acetylcholine from plexus neurons, gastrin from gastrin releasing cells and histamine from ECl cells. Once food reaches stomach, gastric phase stimuli- distention from volume of ingested material and presence of peptides and amino acids released by digestion of luminal proteins- produce an increase in HCl secretion.
Ulcer formation involves breaking the mucosal barrier and exposing the underlying tissue to the corrosive action of acid and pepsin. The walls of stomach are protected from digestion by the presence of alkaline mucus, tight junction between epithelial cells and rapid replacement of damaged epithelial cells. Many factors, including genetic susceptibility, drugs, alcohol, bile salts and excessive secretion of acid and pepsin may contribute to ulcer formation. The major factor, however, is the presence of bacterium, Helicobacter pylori, that is present in stomach of majority of patients with ulcers. Suppression of these bacteria with antibiotics usually helps heal the damaged mucosa.
Primary H+/K+ ATPases in the luminal membrane of the parietal cells pump these hydrogen ions into the lumen of the stomach. H+ is secreted into the lumen, HCO3- is secreted on the opposite side of the cell into the blood in exchange for Cl- . Removal of the end products of this reaction enhances forward rate of reaction. In this way, production and secretion of H+ are coupled. Increased acid secretion results from the transfer of H+/K+ ATPases proteins from the membranes of intracellular vesicles to the plasma membrane by fusion of these vesicles with the membrane, thereby increasing the number of pump proteins in plasma membrane.
Four chemical messengers regulate the insertion of H+/K+ ATPases into the plasma membrane and therefore acid secretion : gastrin, acetylcholine, histamine and somatostatin. Somatostatin inhibits acid secretion, where other three stimulate secretion.
Cephalic and gastric phase also control secretion of HCl. During Cephalic phase, increased activity of efferent parasympathetic neural input to the stomach's enteric nervous system results in the release of acetylcholine from plexus neurons, gastrin from gastrin releasing cells and histamine from ECl cells. Once food reaches stomach, gastric phase stimuli- distention from volume of ingested material and presence of peptides and amino acids released by digestion of luminal proteins- produce an increase in HCl secretion.
Ulcer formation involves breaking the mucosal barrier and exposing the underlying tissue to the corrosive action of acid and pepsin. The walls of stomach are protected from digestion by the presence of alkaline mucus, tight junction between epithelial cells and rapid replacement of damaged epithelial cells. Many factors, including genetic susceptibility, drugs, alcohol, bile salts and excessive secretion of acid and pepsin may contribute to ulcer formation. The major factor, however, is the presence of bacterium, Helicobacter pylori, that is present in stomach of majority of patients with ulcers. Suppression of these bacteria with antibiotics usually helps heal the damaged mucosa.
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