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Gastric acid orstomach acid is theacidic component –hydrochloric acid – ofgastric juice, produced byparietal cells in thegastric glands of thestomach lining. In humans, thepH is between one and three, much lower than most other animals, but is very similar to that ofcarrion-eatingcarnivores that need protection from ingestingpathogens.[1]
With this higher acidity, gastric acid plays a key protective role against pathogens. It is also key in thedigestion ofproteins by activatingdigestive enzymes, which together break down thelong chains of amino acids. Gastric acid is regulated in feedback systems to increase production when needed, such as after a meal. Other cells in thestomach producebicarbonate, a base, tobuffer the fluid, ensuring a regulated pH. These cells also producemucus – aviscous barrier to prevent gastric acid from damaging the stomach. Thepancreas further produces large amounts of bicarbonate, secreting this through thepancreatic duct to theduodenum to neutralize gastric acid passing into thedigestive tract.
The secretion is a complex and relatively energetically expensive process. Parietal cells contain an extensive secretory network (calledcanaliculi) from which the hydrochloric acid is secreted into thelumen of the stomach. The pH level is maintained by theproton pumpH+/K+ ATPase.[2] The parietal cell releasesbicarbonate into the bloodstream in the process, which causes a temporary rise of pH in the blood, known as analkaline tide.
The gastric juice also containsdigestive enzymes produced by other cells in the gastric glands –gastric chief cells. Gastric chief cells secrete an inactivatedpepsinogen. Once in the stomach lumen gastric acid activates the proenzyme topepsin.
A typical adult human stomach will secrete about 1.5 liters ofgastric juice daily.[3] Gastric juice is the combination ofgastric gland secretions including the main component ofhydrochloric acid (gastric acid),gastric lipase andpepsinogen.[4] Once in the stomach pepsinogen is changed by gastric acid to the digestive enzymepepsin adding this enzyme to the gastric juice.[5] In humans, thepH of gastric acid is between one and three, much lower than most other animals, but is very similar to that ofcarrion eatingcarnivores, needing extra protection from ingestingpathogens.[1][6]
Gastric acid secretion is produced in several steps. Chloride and hydrogenions are secreted separately from the cytoplasm ofparietal cells and mixed in the canaliculi. This creates anegative potential of between −40 and −70 mV across the parietal cell membrane that causes potassium ions and a small number of sodium ions todiffuse from the cytoplasm into the parietal cell canaliculi. Gastric acid is then secreted along with other gland secretions into thegastric pit for release into the stomach lumen.[3]
The enzymecarbonic anhydrase catalyses the reaction between carbon dioxide and water to formcarbonic acid. This acid immediately dissociates into hydrogen and bicarbonate ions. The hydrogen ions leave the cell throughH+/K+ ATPaseantiporter pumps.
At the same time, sodium ions are actively reabsorbed.[citation needed] 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 theoxyntic gland.
The highest concentration that gastric acid reaches in the stomach is 160 mM in the canaliculi. This is about 3 million times that ofarterialblood, but almost exactlyisotonic with other bodily fluids. The lowest pH of the secreted acid is 0.8,[7] but the acid is diluted in the stomach lumen to a pH of between 1 and 3.
There is a small continuous basal secretion of gastric acid between meals of usually less than 10 mEq/hour.[8]
There are three phases in the secretion of gastric acid which increase the secretion rate in order to digest a meal:[3]
Gastric acid production is regulated by both theautonomic nervous system and severalhormones. Theparasympathetic nervous system, via thevagus nerve, and the hormonegastrin stimulate the parietal cell to produce gastric acid, both directly acting on parietal cells and indirectly, through the stimulation of the secretion of the hormonehistamine fromenterochromaffin-like cells (ECLs).Vasoactive intestinal peptide,cholecystokinin, andsecretin all inhibit production.
The production of gastric acid in the stomach is tightly regulated by positive regulators andnegative feedback mechanisms. Four types of cells are involved in this process: parietal cells,G cells,D cells 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 stimulatoryneurotransmitters:acetylcholine[10] andgastrin-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 bysomatostatin.[11]
In theduodenum, gastric acid isneutralized bybicarbonate. This also blocks gastric enzymes that function optimally in the acid range ofpH. The secretion of bicarbonate from thepancreas is stimulated bysecretin. Thispolypeptide hormone gets activated and secreted from so-calledS cells in the mucosa of the duodenum andjejunum when the pH in the duodenum falls below 4.5 to 5.0. The neutralization is described by the equation:
Thecarbonic acid rapidly equilibrates withcarbon dioxide andwater through catalysis by carbonic anhydrase enzymes bound to the gut epithelial lining,[12] 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.
Gastroesophageal reflux disease (GERD) is a common disorder that occurs when stomach acid repeatedly flows back into theesophagus, this backwash of acid (reflux) also known asheartburn can irritate the lining of the esophagus. Most people are able to manage the discomfort of GERD with lifestyle changes and medications, notablyproton pump inhibitors, andH2 blockers. Antacids may also be used to neutralise gastric acid. Sometimes, surgery may be needed to ease symptoms.[13]
Chronic inflammation of the gastric mucosa can lead toatrophic gastritis resulting in a decreased secretion of gastric acid, and consequent digestive problems.
Inhypochlorhydria andachlorhydria, gastric acid is either low or absent, respectively. This can potentially lead to less protection against ingested pathogens such asVibrio orHelicobacterbacteria.
InZollinger–Ellison syndromegastrin levels are increased, leading to excess gastric acid production, which can causegastric ulcers.[14]Hypercalcemia also increases gastrin and gastric acid and can cause ulcers.[15]
In diseases featuring excess vomiting,hypochloremicmetabolic alkalosis (decreased blood acidity byH+ andchlorine depletion) may develop.
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The role of gastric acid indigestion was established in the 1820s and 1830s byWilliam Beaumont onAlexis St. Martin, who, as a result of an accident, had afistula (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.[16]
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