Gastric acid

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Determinants of Gastric Acid Secretion
Determinants of gastric acid secretion

Gastric acid, gastric juice, or stomach acid is a digestive fluid formed within the

buffer the fluid, ensuring a regulated pH. These cells also produce mucus – a viscous barrier to prevent gastric acid from damaging the stomach. The pancreas further produces large amounts of bicarbonate and secretes bicarbonate through the pancreatic duct to the duodenum to neutralize gastric acid passing into the digestive tract
.

The primary active component of gastric acid is

canaliculi) from which the "hydrochloric acid" is secreted into the lumen of the stomach. The pH of gastric acid is 1.5 to 3.5 in the human stomach lumen, a level maintained by the proton pump H+/K+ ATPase.[1] 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 highly acidic environment in the stomach lumen degrades

rennin). The low pH activates pepsinogen into the enzyme pepsin, which then aids digestion by breaking the amino acid bonds, a process called proteolysis. In addition, many microorganisms are inhibited or destroyed in an acidic environment, preventing infection
or sickness.

Secretion

A typical adult human stomach will secrete about 1.5 liters of gastric acid daily.

gastric gland and gradually reaches the main stomach lumen.[2]
The exact manner in which the secreted acid reaches the stomach lumen is controversial, as acid must first cross the relatively pH-neutral gastric mucus layer.

Chloride and sodium ions are secreted actively from the

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. The hydrogen ions leave the cell through H+/K+ ATPase antiporter pumps.

At the same time, sodium ions are actively reabsorbed[

oxyntic gland
.

The highest concentration that gastric acid reaches in the stomach is 160 

isotonic with other bodily fluids. The lowest pH of the secreted acid is 0.8,[3]
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.[4]

There are three phases in the secretion of gastric acid which increase the secretion rate in order to digest a meal:[2]

  1. The
    D cells.[5]
  2. The
    amino acids
    present in the food.
  3. The
    amino acids. The duodenal cells release entero-oxyntin which acts on parietal cells without affecting gastrin.[5]

Regulation of secretion

See also:
Regulation of gastric function
Diagram depicting the major determinants of gastric acid secretion, with inclusion of drug targets for peptic ulcer disease (PUD) and gastroesophageal reflux disease (GERD).

Gastric acid production is regulated by both the

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

D cells
and enterochromaffine-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 neurotransmitters: acetylcholine[6] 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 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.[7]

Neutralization

In the

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 4.5 to 5.0. The neutralization is described by the equation:

HCl + NaHCO3 → NaCl + H2CO3

The

water through catalysis by carbonic anhydrase enzymes bound to the gut epithelial lining,[8]
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.

Role in disease

In

digestive tract (such as infection with Vibrio or Helicobacter
bacteria).

In

gastric ulcers
.

In diseases featuring excess vomiting, patients develop hypochloremic metabolic alkalosis (decreased blood acidity by H+ and chlorine depletion).

Gastroesophageal reflux disease occurs when stomach acid repeatedly flows back into the Esophagus, this backwash (acid reflux) can irritate the lining of the esophagus.

Many people experience acid reflux from time to time. However, when acid reflux happens repeatedly over time, it can cause GERD.

Most people are able to manage the discomfort of GERD with lifestyle changes and medications. While it is uncommon, some may need surgery to ease symptoms.[9]

Pharmacology

The proton pump enzyme is the target of

H2 antagonists indirectly decrease gastric acid production. Antacids
neutralize existing acid.

Comparison between humans and other animals

The pH of gastric acid in humans is 1.5-2.0. This is a much lower pH level than that of most animals and very close to scavengers, which eat carrion.[10] This suggests that carrion feeding could have been more important in human evolution than previously thought.[10]

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.[11]

See also

References

  1. ISBN 978-0-13-458099-9
    .
  2. ^ a b c Dworken HJ (2016). Human digestive system: gastric secretion. Encyclopædia Britannica Inc.
  3. ISBN 0-7216-0240-1
    .
  4. ISBN 978-0-7817-7153-5
    .
  5. ^ a b Lecture, "Function of the Stomach and Small Intestine" Deakin University School of Medicine. October 15, 2012
  6. ^ "acetylcholine | Definition, Function, & Facts | Britannica". www.britannica.com. Retrieved 2021-12-13.
  7. ^ "Somatostatin". www.hormone.org. Retrieved 2021-12-13.
  8. PMID 2506730
    .
  9. ^ "Gastroesophageal reflux disease (GERD) - Symptoms and causes". Mayo Clinic. Retrieved 2023-09-10.
  10. ^
    PMID 26222383
    .
  11. ISBN 0-7148-2096-2
    .

External links

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