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Gastric acid or stomach acid is the component – hydrochloric acid – of gastric juice, produced by in the gastric glands of the gastric mucosa. In humans, the pH is between one and three, much lower than most other animals, but is very similar to that of carrion-eating that need protection from ingesting .
With this higher acidity, gastric acid plays a key protective role against pathogens. It is also key in the digestion of by activating , which together break down the long chains of amino acids. Gastric acid is regulated in feedback systems to increase production when needed, such as after a meal. Other cells in the stomach produce bicarbonate, a base, to Buffering agent the fluid, ensuring a regulated pH. These cells also produce mucus – a viscosity barrier to prevent gastric acid from damaging the stomach. The pancreas further produces large amounts of bicarbonate, secreting this through the pancreatic duct to the duodenum to neutralize gastric acid passing into the digestive tract.
The secretion is a complex and relatively energetically expensive process. Parietal cells contain an extensive secretory network (called canaliculi) from which the hydrochloric acid is secreted into the lumen of the stomach. The pH level is maintained by the proton pump H+/K+ ATPase. The parietal cell releases bicarbonate into the bloodstream in the process, which causes a temporary rise of pH in the blood, known as an alkaline tide.
The gastric juice also contains produced by other cells in the gastric glands – gastric chief cells. Gastric chief cells secrete an inactivated pepsinogen. Once in the stomach lumen gastric acid activates the proenzyme to pepsin.
Gastric acid secretion is produced in several steps. Chloride and hydrogen are secreted separately from the cytoplasm of and mixed in the canaliculi. This creates a negative potential of between −40and−70millivolt across the parietal cell membrane that causes potassium ions and a small number of sodium ions to diffusion from the cytoplasm into the parietal cell canaliculi. Gastric acid is then secreted along with other gland secretions into the gastric pit for release into the stomach lumen.
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. The hydrogen ions leave the cell through H+/K+ ATPase antiporter pumps.
At the same time, sodium ions are actively reabsorbed . This means that the majority of secreted K+ (potassium) and Na+ (sodium) ions return to the cytoplasm. 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 160millimolar in the canaliculi. This is about 3 million times that of artery blood, but almost exactly Isotonicity with other bodily fluids. The lowest pH of the secreted acid is 0.8,
There is a small continuous basal secretion of gastric acid between meals of usually less than 10mEq/hour.Page 192 in:
There are three phases in the secretion of gastric acid which increase the secretion rate in order to digest a meal:
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: parietal cells, , Delta cell and enterochromaffin-like cells. Beside 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 : acetylcholine and gastrin-releasing peptide. Their action is both direct on parietal cells and mediated through the secretion of gastrin from G cells and histamine from enterochromaffin-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.
The carbonic acid rapidly equilibrates with carbon dioxide and water through catalysis by carbonic anhydrase enzymes bound to the gut epithelial lining, leading to a net release of carbon dioxide gas within the lumen associated with neutralisation. 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.
Chronic inflammation of the gastric mucosa can lead to atrophic gastritis resulting in a decreased secretion of gastric acid, and consequent digestive problems.
In hypochlorhydria and achlorhydria, gastric acid is either low or absent, respectively. This can potentially lead to less protection against ingested pathogens such as Vibrio or Helicobacter bacteria.
In Zollinger–Ellison syndrome gastrin levels are increased, leading to excess gastric acid production, which can cause .
Hypercalcemia also increases gastrin and gastric acid and can cause ulcers.
In diseases featuring excess vomiting, chlorine metabolic alkalosis (decreased blood acidity by hydrogen+ and chlorine depletion) may develop.
(2025). 9780721602400, Elsevier Saunders. ISBN 9780721602400 but the acid is diluted in the stomach lumen to a pH of between 1 and 3.
Regulation of secretion
Gastric acid production is regulated by both the autonomic nervous system and several . 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 enterochromaffin-like cells (ECLs). Vasoactive intestinal peptide, cholecystokinin, and secretin all inhibit production.
Neutralization
In the duodenum, gastric acid is neutralized by bicarbonate. This also blocks gastric enzymes that function optimally in the acid range of pH. The secretion of bicarbonate from the pancreas is stimulated by secretin. This polypeptide hormone gets activated and secreted from so-called in the mucosa of the duodenum and jejunum when the pH in the duodenum falls below 4.5 to 5.0. The neutralization is described by the equation:
Clinical significance
Gastroesophageal reflux disease (GERD) is a common disorder that occurs when stomach acid repeatedly flows back into the esophagus, this backwash of acid (reflux) also known as heartburn can irritate the lining of the esophagus. Most people are able to manage the discomfort of GERD with lifestyle changes and medications, notably proton pump inhibitors, and H2 blockers. Antacids may also be used to neutralise gastric acid. Sometimes, surgery may be needed to ease symptoms.
History
The role of gastric acid in digestion was established in the 1820s and 1830s by William Beaumont on Alexis St. Martin, who, as a result of an accident, had a fistula (hole) in his stomach, which allowed Beaumont to observe the process of digestion and to extract gastric acid, verifying that acid played a crucial role in digestion.
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