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Structure Of The Stomach - Functions Of The Stomach - How Does The Stomach Work
Secretion[ edit ] A typical adult human stomach will secrete about 1. Chloride and hydrogen ions are secreted separately from the cytoplasm of parietal cells and mixed in the canaliculi. Gastric acid is then secreted into the lumen of the gastric gland and gradually reaches the main stomach lumen. Chloride and sodium ions are secreted actively from the cytoplasm of the parietal cell into the lumen of the canaliculus. This creates a negative potential of m V to mV across the parietal cell membrane that causes potassium ions and a small number of sodium ions to diffuse from the cytoplasm into the parietal cell canaliculi. The enzyme carbonic anhydrase catalyses the reaction between carbon dioxide and water to form carbonic acid. This acid immediately dissociates into hydrogen and bicarbonate ions. At the same time, sodium ions are actively reabsorbed. In the canaliculus, secreted hydrogen and chloride ions mix and are secreted into the lumen of the oxyntic gland. The highest concentration that gastric acid reaches in the stomach is mM in the canaliculi. This is about 3 million times that of arterial blood , but almost exactly isotonic with other bodily fluids. The lowest pH of the secreted acid is 0. Thirty percent of the total gastric acid secretions to be produced is stimulated by anticipation of eating and the smell or taste of food. This signalling occurs from higher centres in the brain through the vagus nerve Cranial Nerve X. It activates parietal cells to release acid and ECL cells to release histamine. The vagus nerve CN X also releases gastrin releasing peptide onto G cells. Finally, it also inhibits somatostatin release from D cells. About sixty percent of the total acid for a meal is secreted in this phase. Acid secretion is stimulated by distension of the stomach and by amino acids present in the food. The duodenal cells release entero-oxyntin which acts on parietal cells without affecting gastrin. Gastric acid production is regulated by both the autonomic nervous system and several hormones. The parasympathetic nervous system , via the vagus nerve , and the hormone gastrin stimulate the parietal cell to produce gastric acid, both directly acting on parietal cells and indirectly, through the stimulation of the secretion of the hormone histamine from enterochromaffine-like cells ECL. Vasoactive intestinal peptide , cholecystokinin , and secretin all inhibit production. The production of gastric acid in the stomach is tightly regulated by positive regulators and negative feedback mechanisms. Four types of cells are involved in this process: Besides this, the endings of the vagus nerve CN X and the intramural nervous plexus in the digestive tract influence the secretion significantly. Nerve endings in the stomach secrete two stimulatory neurotransmitters: Their action is both direct on parietal cells and mediated through the secretion of gastrin from G cells and histamine from enterochromaffine-like cells. Gastrin acts on parietal cells directly and indirectly too, by stimulating the release of histamine. The release of histamine is the most important positive regulation mechanism of the secretion of gastric acid in the stomach. Its release is stimulated by gastrin and acetylcholine and inhibited by somatostatin. Neutralization[ edit ] In the duodenum , gastric acid is neutralized by sodium bicarbonate. This also blocks gastric enzymes that have their optima in the acid range of pH. The secretion of sodium bicarbonate from the pancreas is stimulated by secretin. This polypeptide hormone gets activated and secreted from so-called S cells in the mucosa of the duodenum and jejunum when the pH in the duodenum falls below 4. The neutralization is described by the equation: In the absorptive upper intestine, such as the duodenum, both the dissolved carbon dioxide and carbonic acid will tend to equilibrate with the blood, leading to most of the gas produced on neutralisation being exhaled through the lungs. Role in disease[ edit ] In hypochlorhydria and achlorhydria , there is low or no gastric acid in the stomach, potentially leading to problems as the disinfectant properties of the gastric lumen are decreased. In such conditions, there is greater risk of infections of the digestive tract such as infection with Vibrio or Helicobacter bacteria. In Zollinger—Ellison syndrome and hypercalcemia , there are increased gastrin levels, leading to excess gastric acid production, which can cause gastric ulcers. Pharmacology[ edit ] The proton pump enzyme is the target of proton pump inhibitors , used to increase gastric pH and hence decrease stomach acidity in diseases that feature excess acid. H2 antagonists indirectly decrease gastric acid production. Antacids neutralize existing acid.
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