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Gastric acid
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<h2 id="secretion">Secretion</h2> <p>A typical adult human stomach will secrete about 1.5 liters of <a href="/facts/Gastric_juice/btVCyhYH">gastric juice</a> daily.<a class="footnote-ref" id="fnref:3" href="#fn:3"><sup>3</sup></a> Gastric juice is the combination of <a href="/facts/Gastric_gland/SQv79wXT">gastric gland</a> secretions including the main component of <a href="/facts/Hydrochloric_acid/HqItJlUT">hydrochloric acid</a> (gastric acid), <a href="/facts/Gastric_lipase/DNBp2czj">gastric lipase</a> and <a href="/facts/Pepsinogen/pELlV241">pepsinogen</a>.<a class="footnote-ref" id="fnref:4" href="#fn:4"><sup>4</sup></a> Once in the stomach pepsinogen is changed by gastric acid to the digestive enzyme <a href="/facts/Pepsin/pELlV241">pepsin</a> adding this enzyme to the gastric juice.<a class="footnote-ref" id="fnref:5" href="#fn:5"><sup>5</sup></a> In humans, the <a href="/facts/PH/RnSv8D7y">pH</a> of gastric acid is between one and three, much lower than most other animals, but is very similar to that of <a href="/facts/Carrion/rpAgjBY6">carrion</a> eating <a href="/facts/Carnivore/q6h6aSqe">carnivores</a>, needing extra protection from ingesting <a href="/facts/Pathogen/axMXtV1M">pathogens</a>.<a class="footnote-ref" id="fnref:6" href="#fn:6"><sup>6</sup></a><a class="footnote-ref" id="fnref:7" href="#fn:7"><sup>7</sup></a> </p><p>Gastric acid secretion is produced in several steps. Chloride and hydrogen <a href="/facts/Ion/wrbwhF3z">ions</a> are secreted separately from the cytoplasm of <a href="/facts/Parietal_cell/jS1nXJnw">parietal cells</a> and mixed in the canaliculi. This creates a <a href="/facts/Transmembrane_potential_difference/DpNG14c7">negative potential</a> of between −40 and −70 <a href="/facts/Millivolt/KF18MXP2">mV</a> across the parietal cell membrane that causes potassium ions and a small number of sodium ions to <a href="/facts/Diffusion/KbAxroBa">diffuse</a> from the cytoplasm into the parietal cell canaliculi. Gastric acid is then secreted along with other gland secretions into the <a href="/facts/Gastric_pit/Y45xDPb7">gastric pit</a> for release into the stomach lumen.<a class="footnote-ref" id="fnref:8" href="#fn:8"><sup>8</sup></a> </p><p>The enzyme <a href="/facts/Carbonic_anhydrase/je7bk6fk">carbonic anhydrase</a> catalyses the reaction between carbon dioxide and water to form <a href="/facts/Carbonic_acid/fjjVAhwt">carbonic acid</a>. This acid immediately dissociates into hydrogen and bicarbonate ions. The hydrogen ions leave the cell through <a href="/facts/Hydrogen_potassium_ATPase/8fbvtrRP">H+/K+ ATPase</a> <a href="/facts/Antiporter/HHMvokyn">antiporter</a> pumps. </p><p>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 <a href="/facts/Oxyntic_gland/SQv79wXT">oxyntic gland</a>. </p><p>The highest concentration that gastric acid reaches in the stomach is 160 <a href="/facts/Millimolar/P2WL5b9q">mM</a> in the canaliculi. This is about 3 million times that of <a href="/facts/Artery/Y1Yj0jat">arterial</a> <a href="/facts/Blood/03zEulkj">blood</a>, but almost exactly <a href="/facts/Isotonicity/ev5qcKQh">isotonic</a> with other bodily fluids. The lowest pH of the secreted acid is 0.8,<a class="footnote-ref" id="fnref:9" href="#fn:9"><sup>9</sup></a> but the acid is diluted in the stomach lumen to a pH of between 1 and 3. </p><p>There is a small continuous basal secretion of gastric acid between meals of usually less than 10 mEq/hour.<a class="footnote-ref" id="fnref:10" href="#fn:10"><sup>10</sup></a> </p><p>There are three phases in the secretion of gastric acid which increase the secretion rate in order to digest a meal:<a class="footnote-ref" id="fnref:11" href="#fn:11"><sup>11</sup></a> </p> <ol><li>The <a href="/facts/Cephalic_phase/IIafq8Hj">cephalic phase</a>: 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 <a href="/facts/Vagus_Nerve/cKQR0rLm">vagus nerve (Cranial Nerve X)</a>. It activates <a href="/facts/Parietal_cells/jS1nXJnw">parietal cells</a> to release acid and <a href="/facts/ECL_cells/eJ6WBFo3">ECL cells</a> to release <a href="/facts/Histamine/Vfjda665">histamine</a>. The vagus nerve (CN X) also releases <a href="/facts/Gastrin_Releasing_Peptide/TKJssgWn">gastrin releasing peptide</a> onto <a href="/facts/G_cells/YuPPW4Ig">G cells</a>. Finally, it also inhibits <a href="/facts/Somatostatin/GAD2utoz">somatostatin</a> release from <a href="/facts/D_cells/dS2tDQVx">D cells</a>.<a class="footnote-ref" id="fnref:12" href="#fn:12"><sup>12</sup></a></li> <li>The <a href="/facts/Gastric_phase/IIafq8Hj">gastric phase</a>: 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 <a href="/facts/Amino_acids/WDxYwBny">amino acids</a> present in the food.</li> <li>The <a href="/facts/Intestinal_phase/IIafq8Hj">intestinal phase</a>: The remaining 10% of acid is secreted when <a href="/facts/Chyme/zty06x48">chyme</a> enters the small intestine, and is stimulated by small intestine distension and by <a href="/facts/Amino_acids/WDxYwBny">amino acids</a>. The duodenal cells release <a href="/facts/Entero-oxyntin/Pvaadn7q">entero-oxyntin</a> which acts on parietal cells without affecting gastrin.<a class="footnote-ref" id="fnref:13" href="#fn:13"><sup>13</sup></a></li></ol> <h2 id="regulation-of-secretion">Regulation of secretion</h2> <p class="note">See also: <a href="/facts/Phases_of_digestion/IIafq8Hj">Phases of digestion</a></p> <p>Gastric acid production is regulated by both the <a href="/facts/Autonomic_nervous_system/hdmEY1Ay">autonomic nervous system</a> and several <a href="/facts/Hormone/WFnBnINJ">hormones</a>. The <a href="/facts/Parasympathetic_nervous_system/eNzCI8Yu">parasympathetic nervous system</a>, via the <a href="/facts/Vagus_nerve/cKQR0rLm">vagus nerve</a>, and the hormone <a href="/facts/Gastrin/C4a4VSbz">gastrin</a> 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 <a href="/facts/Histamine/Vfjda665">histamine</a> from <a href="/facts/Enterochromaffin-like_cell/eJ6WBFo3">enterochromaffin-like cells</a> (ECLs). <a href="/facts/Vasoactive_intestinal_peptide/KFsEElwE">Vasoactive intestinal peptide</a>, <a href="/facts/Cholecystokinin/VILtAKuT">cholecystokinin</a>, and <a href="/facts/Secretin/M77lRJbo">secretin</a> all inhibit production. </p><p>The production of gastric acid in the stomach is tightly regulated by positive regulators and <a href="/facts/Negative_feedback/G9byVgpN">negative feedback</a> mechanisms. Four types of cells are involved in this process: parietal cells, <a href="/facts/G_cell/YuPPW4Ig">G cells</a>, <a href="/facts/Delta_cell/dS2tDQVx">D cells</a> 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. </p><p>Nerve endings in the stomach secrete two stimulatory <a href="/facts/Neurotransmitter/LlpYFSU3">neurotransmitters</a>: <a href="/facts/Acetylcholine/v1d3wRUd">acetylcholine</a><a class="footnote-ref" id="fnref:14" href="#fn:14"><sup>14</sup></a> and <a href="/facts/Gastrin-releasing_peptide/TKJssgWn">gastrin-releasing peptide</a>. 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. </p><p>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 <a href="/facts/Somatostatin/GAD2utoz">somatostatin</a>.<a class="footnote-ref" id="fnref:15" href="#fn:15"><sup>15</sup></a> </p> <h2 id="neutralization">Neutralization</h2> <p>In the <a href="/facts/Duodenum/IAIgHBmq">duodenum</a>, gastric acid is <a href="/facts/Neutralization_(chemistry)/WC1c5fj1">neutralized</a> by <a href="/facts/Sodium_bicarbonate/S9oSol0R">bicarbonate</a>. This also blocks gastric enzymes that function optimally in the acid range of <a href="/facts/PH/RnSv8D7y">pH</a>. The secretion of bicarbonate from the <a href="/facts/Pancreas/r0WPGjAq">pancreas</a> is stimulated by <a href="/facts/Secretin/M77lRJbo">secretin</a>. This <a href="/facts/Polypeptide/C4ltc7UG">polypeptide</a> hormone gets activated and secreted from so-called <a href="/facts/S_cell/AqECJKf9">S cells</a> in the mucosa of the duodenum and <a href="/facts/Jejunum/PU0q1Syr">jejunum</a> when the pH in the duodenum falls below 4.5 to 5.0. The neutralization is described by the equation: </p> HCl + NaHCO3 → NaCl + H2CO3 <p>The <a href="/facts/Carbonic_acid/fjjVAhwt">carbonic acid</a> rapidly equilibrates with <a href="/facts/Carbon_dioxide/xGzpppEp">carbon dioxide</a> and <a href="/facts/Water_(molecule)/FFsl65l1">water</a> through catalysis by carbonic anhydrase enzymes bound to the gut epithelial lining,<a class="footnote-ref" id="fnref:16" href="#fn:16"><sup>16</sup></a> 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. </p> <h2 id="clinical-significance">Clinical significance</h2> <p><a href="/facts/Gastroesophageal_reflux_disease/8YhncnDz">Gastroesophageal reflux disease</a> (GERD) is a common disorder that occurs when stomach acid repeatedly flows back into the <a href="/facts/Esophagus/XWa7WoWn">esophagus</a>, this backwash of acid (reflux) also known as <a href="/facts/Heartburn/MkNPKoxS">heartburn</a> can irritate the lining of the esophagus. Most people are able to manage the discomfort of GERD with lifestyle changes and medications, notably <a href="/facts/Proton_pump_inhibitor/JIpwabbk">proton pump inhibitors</a>, and <a href="/facts/H2_blocker/Ra6UHBGy">H2 blockers</a>. Antacids may also be used to neutralise gastric acid. Sometimes, surgery may be needed to ease symptoms.<a class="footnote-ref" id="fnref:17" href="#fn:17"><sup>17</sup></a> </p><p>Chronic inflammation of the gastric mucosa can lead to <a href="/facts/Atrophic_gastritis/foxs959P">atrophic gastritis</a> resulting in a decreased secretion of gastric acid, and consequent digestive problems. </p><p>In <a href="/facts/Hypochlorhydria/s34xesR6">hypochlorhydria</a> and <a href="/facts/Achlorhydria/s34xesR6">achlorhydria</a>, gastric acid is either low or absent, respectively. This can potentially lead to less protection against ingested pathogens such as <i><a href="/facts/Vibrio/Lkef6ynj">Vibrio</a></i> or <i><a href="/facts/Helicobacter/EYzbnhTU">Helicobacter</a></i> <a href="/facts/Bacteria/wC8xSCsU">bacteria</a>. </p><p>In <a href="/facts/Zollinger%25E2%2580%2593Ellison_syndrome/qrI4NkPa">Zollinger–Ellison syndrome</a> <a href="/facts/Gastrin/C4a4VSbz">gastrin</a> levels are increased, leading to excess gastric acid production, which can cause <a href="/facts/Gastric_ulcer/peMGnYCd">gastric ulcers</a>.<a class="footnote-ref" id="fnref:18" href="#fn:18"><sup>18</sup></a> <a href="/facts/Hypercalcemia/kdEeLaVd">Hypercalcemia</a> also increases gastrin and gastric acid and can cause ulcers.<a class="footnote-ref" id="fnref:19" href="#fn:19"><sup>19</sup></a> </p><p>In diseases featuring excess vomiting, <a href="/facts/Chlorine/y27UwYBM">hypochloremic</a> <a href="/facts/Metabolic_alkalosis/M4KlT5b7">metabolic alkalosis</a> (decreased blood acidity by <a href="/facts/Hydrogen/BoYHjl0J">H</a>+ and <a href="/facts/Chlorine/y27UwYBM">chlorine</a> depletion) may develop. </p> <h2 id="history">History</h2> <p>The role of gastric acid in <a href="/facts/Digestion/sjUBmhBS">digestion</a> was established in the 1820s and 1830s by <a href="/facts/William_Beaumont/wrcjnbpn">William Beaumont</a> on <a href="/facts/Alexis_St._Martin/JGR2nhgK">Alexis St. Martin</a>, who, as a result of an accident, had a <a href="/facts/Fistula/xlRcRGCJ">fistula</a> (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.<a class="footnote-ref" id="fnref:20" href="#fn:20"><sup>20</sup></a> </p> <h2 id="see-also">See also</h2> <ul><li><a href="/facts/Discovery_and_development_of_proton_pump_inhibitors/1DUwJe2R">Discovery and development of proton pump inhibitors</a></li></ul> <h2 id="external-links">External links</h2> Wikimedia Commons has media related to Gastric acid. <ul><li><a href="http://www.vivo.colostate.edu/hbooks/pathphys/digestion/stomach/parietal.html">The Parietal Cell: Mechanism of Acid Secretion; Colorado State University</a></li></ul> <h2 id="references">References</h2> <ol> <li id="fn:1"><p>Fujimori, S (21 November 2020). "Gastric acid level of humans must decrease in the future". World Journal of Gastroenterology. 26 (43): 6706–6709. doi:10.3748/wjg.v26.i43.6706. PMC 7684463. PMID 33268958. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7684463" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7684463</a> <a href="#fnref:1" class="footnote-back-ref">↩</a></p></li> <li id="fn:2"><p>Marieb EN, Hoehn K (2018). Human Anatomy and Physiology (11th ed.). Pearson Education. p. 1264. ISBN 978-0-13-458099-9. <a href="978-0-13-458099-9" target="_blank">978-0-13-458099-9</a> <a href="#fnref:2" class="footnote-back-ref">↩</a></p></li> <li id="fn:3"><p>Dworken HJ (2016). Human digestive system: gastric secretion. Encyclopædia Britannica Inc. <a href="https://www.britannica.com/science/human-digestive-system/Gastric-secretion" target="_blank">https://www.britannica.com/science/human-digestive-system/Gastric-secretion</a> <a href="#fnref:3" class="footnote-back-ref">↩</a></p></li> <li id="fn:4"><p>Martinsen TC, Fossmark R, Waldum HL (November 2019). "The Phylogeny and Biological Function of Gastric Juice-Microbiological Consequences of Removing Gastric Acid". Int J Mol Sci. 20 (23): 6031. doi:10.3390/ijms20236031. PMC 6928904. PMID 31795477. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6928904" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6928904</a> <a href="#fnref:4" class="footnote-back-ref">↩</a></p></li> <li id="fn:5"><p>Sehgal, Shalini; Saji, Hephzibah; Banik, Samudra Prosad (1 January 2022). "Chapter 11 - Role of food structure in digestion and health". Nutrition and Functional Foods in Boosting Digestion, Metabolism and Immune Health: 151–165. doi:10.1016/B978-0-12-821232-5.00019-7. ISBN 978-0-12-821232-5. <a href="978-0-12-821232-5" target="_blank">978-0-12-821232-5</a> <a href="#fnref:5" class="footnote-back-ref">↩</a></p></li> <li id="fn:6"><p>Fujimori, S (21 November 2020). "Gastric acid level of humans must decrease in the future". World Journal of Gastroenterology. 26 (43): 6706–6709. doi:10.3748/wjg.v26.i43.6706. PMC 7684463. PMID 33268958. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7684463" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7684463</a> <a href="#fnref:6" class="footnote-back-ref">↩</a></p></li> <li id="fn:7"><p>Beasley DE, Koltz AM, Lambert JE, Fierer N, Dunn RR (2015-07-29). "The Evolution of Stomach Acidity and Its Relevance to the Human Microbiome". PLOS ONE. 10 (7): e0134116. Bibcode:2015PLoSO..1034116B. doi:10.1371/journal.pone.0134116. PMC 4519257. 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