in the parietal cells, the enzyme carbonic anhydrase causes a reaction between __________ and __________.

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Digestive System Physiology Lab

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In the parietal cells, the enzyme carbonic anhydrase causes a reaction between...

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carbon dioxide and water.

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Hydrochloric Acid is formed...

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hydrogen ions and chloride ions join in the duct of the gastric gland.

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Essential Cell Biology

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Bruce Alberts, Dennis Bray, Karen Hopkin

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Terms in this set (20)

In the parietal cells, the enzyme carbonic anhydrase causes a reaction between...

carbon dioxide and water.

Hydrochloric Acid is formed...

hydrogen ions and chloride ions join in the duct of the gastric gland.

In the parietal cell, carbonic acid dissociates into a bicarbonate ion and a hydrogen ion.

True.

The carbonic acid ion is joined to a hydrogen ion by the enzyme carbonic anhydrase.

False

The hydrogen ions used to form hydrochloric acid in the stomach are derived from

Carbonic Acid

he ion exchange protein in the plasma membrane of parietal cells exchanges ________ ions going out for ________ ions coming in.

bicarbonate, chloride

________ ions are actively transported into the gastric gland duct, in exchange for ________ ions which enter the parietal cells.

Hydrogen, Potassium

The enzyme carbonic anhydrase catalyzes the formation of bicarbonate from carbon dioxide and hydrogen.

False

Which of the following might stimulate the cephalic phase of gastric secretion?

The thought of food.

Gastric secretion is increased in all three phases (cephalic, gastric, intestinal).

False, only Cephalic

Gastric secretion during the intestinal phase is inhibited by the

presence of lipids or low pH.

Which phase(s) of gastric secretion is (are) regulated by the medulla oblongata?

All three phases are regulated by the Medulla Oblongata.

Which of the following does NOT stimulate the secretion of HCl in the stomach?

Secretin

Secretin is released from the duodenum in response to

hydrochloric acid in chyme.

Which of the following enzymes is produced by the stomach?

Pepsin

When chyme enters the duodenum, gastric secretion increases.

False

Gastrin functions to increase the production of HCl in the stomach.

TRUE

A portal triad consists of which three elements?

Branches of a hepatic artery, hepatic vein, and bile duct

Structurally, the human liver is divided into how many lobes?

4

The liver lobule is the same as a hepatocyte.

False

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The Parietal Cell: Mechanism of Acid Secretion

Vivo Pathophysiology

Digestive System > Stomach

The Parietal Cell: Mechanism of Acid Secretion

The best-known component of gastric juice is hydrochloric acid, the secretory product of the parietal, or oxyntic cell. It is known that the capacity of the stomach to secrete HCl is almost linearly related to parietal cell numbers.

When stimulated, parietal cells secrete HCl at a concentration of roughly 160 mM (equivalent to a pH of 0.8). The acid is secreted into large cannaliculi, deep invaginations of the plasma membrane which are continuous with the lumen of the stomach.

When acid secretion is stimulated there is a dramatic change in the morphology of the membranes of the parietal cell. Cytoplasmic tubulovesicular membranes which are abundant in the resting cell virtually disappear in concert with a large increase in the cannalicular membrane. It appears that the proton pump as well as potassium and chloride conductance channels initially reside on intracellular membranes and are transported to and fused into the cannalicular membrane just prior to acid secretion.

The epithelium of the stomach is intrinsically resistant to the damaging effects of gastric acid and other insults. Nonetheless, excessive secretion of gastric acid is a major problem in human and, to a lesser extent, animal populations, leading to gastritis, gastric ulcers and peptic acid disease. As a consequence, the parietal cell and the mechanisms it uses to secrete acid have been studied extensively, leading to development of several drugs useful for suppressing acid secretion.

Mechanism of Acid Secretion

The hydrogen ion concentration in parietal cell secretions is roughly 3 million fold higher than in blood, and chloride is secreted against both a concentration and electric gradient. Thus, the ability of the partietal cell to secrete acid is dependent on active transport.

The key player in acid secretion is a H+/K+ ATPase or "proton pump" located in the cannalicular membrane. This ATPase is magnesium-dependent, and not inhibitable by ouabain. The current model for explaining acid secretion is as follows:

Hydrogen ions are generated within the parietal cell from dissociation of water. The hydroxyl ions formed in this process rapidly combine with carbon dioxide to form bicarbonate ion, a reaction cataylzed by carbonic anhydrase.

Bicarbonate is transported out of the basolateral membrane in exchange for chloride. The outflow of bicarbonate into blood results in a slight elevation of blood pH known as the "alkaline tide". This process serves to maintain intracellular pH in the parietal cell.

Chloride and potassium ions are transported into the lumen of the cannaliculus by conductance channels, and such is necessary for secretion of acid.

Hydrogen ion is pumped out of the cell, into the lumen, in exchange for potassium through the action of the proton pump; potassium is thus effectively recycled.

Accumulation of osmotically-active hydrogen ion in the cannaliculus generates an osmotic gradient across the membrane that results in outward diffusion of water - the resulting gastric juice is 155 mM HCl and 15 mM KCl with a small amount of NaCl.

A key substrate in the production of gastric acid is CO2, and diffusion of CO2 through the basal surface of the parietal appears to be the rate limiting step in acid synthesis. Interestingly, this biochemical principle has been validated by studying gastric function in alligators. These reptiles produce huge amounts of gastric acid after ingestion of a large carcass, and abundant acid seems to be important in speeding digestion of bone. Alligators have a vascular shunt that diverts CO2-rich venous blood to the stomach rather than directly back to the lungs, increasing the amount of CO2 that diffuses into parietal cells and thereby enhancing synthesis of acid.

Control of Acid Secretion

Parietal cells bear receptors for three stimulators of acid secretion, reflecting a triumverate of neural, paracrine and endocrine control:

Acetylcholine (muscarinic type receptor)GastrinHistamine (H2 type receptor)

Histamine from enterochromaffin-like cells may well be the primary modulator, but the magnitude of the stimulus appears to result from a complex additive or multiplicative interaction of signals of each type. For example, the low amounts of histamine released constantly from mast cells in the gastric mucosa only weakly stimulate acid secretion, and similarly for low levels of gastrin or acetylcholine. However, when low levels of each are present, acid secretion is strongly forced. Additionally, pharmacologic antagonists of each of these molecules can block acid secretion.

Histamine's effect on the parietal cell is to activate adenylate cyclase, leading to elevation of intracellular cyclic AMP concentrations and activation of protein kinase A (PKA). One effect of PKA activation is phosphorylation of cytoskeletal proteins involved in transport of the H+/K+ ATPase from cytoplasm to plasma membrane. Binding of acetylcholine and gastrin both result in elevation of intracellular calcium concentrations.

Source : www.vivo.colostate.edu

Physiology, Pepsin

Food digestion is the breakdown of large food particles into smaller absorbable nutrients needed for energy production, growth, and cellular repair. It begins with ingestion and ends with defecation. Digestion takes place in the gastrointestinal tract in two principal forms: mechanical and chemical. Mechanical digestion is the physical degradation of large food particles into smaller pieces that digestive enzymes can access through chemical digestion. Chemical digestion is the enzymatic cleavage of proteins, carbohydrates, and fats into tiny amino acids, sugars, and fatty acids. Once food enters the mouth, it mixes with saliva and gets chewed through the process of mastication. Saliva is rich in mucus and salivary enzymes, and together, with the effects of mastication, it creates a mass called a food bolus. The food bolus then travels down the esophagus via wave-like muscular contractions, called peristalsis, before it reaches the stomach.

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Physiology, Pepsin

Rajiv Heda; Fadi Toro; Claudio R. Tombazzi.

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Last Update: May 9, 2021.

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Introduction

Food digestion is the breakdown of large food particles into smaller absorbable nutrients needed for energy production, growth, and cellular repair. It begins with ingestion and ends with defecation. Digestion takes place in the gastrointestinal tract in two principal forms: mechanical and chemical. Mechanical digestion is the physical degradation of large food particles into smaller pieces that digestive enzymes can access through chemical digestion. Chemical digestion is the enzymatic cleavage of proteins, carbohydrates, and fats into tiny amino acids, sugars, and fatty acids. Once food enters the mouth, it mixes with saliva and gets chewed through the process of mastication. Saliva is rich in mucus and salivary enzymes, and together, with the effects of mastication, it creates a mass called a food bolus. The food bolus then travels down the esophagus via wave-like muscular contractions, called peristalsis, before it reaches the stomach.

The stomach plays a critical role in the early stages of food digestion. Asides from squeezing and churning the food bolus, it also secretes a mixture of compounds, collectively known as "gastric juice." Gastric juice comprises water, mucus, hydrochloric acid, pepsin, and intrinsic factor. Of these five components, pepsin is the principal enzyme involved in protein digestion. It breaks down proteins into smaller peptides and amino acids that can be easily absorbed in the small intestine. Specific cells within the gastric lining, known as chief cells, release pepsin in an inactive form, or zymogen form, called pepsinogen. By doing so, the stomach prevents the auto-digestion of protective proteins in the lining of the digestive tract. Since chief cells release pepsin as a zymogen, activation by an acidic environment is necessary. Hydrochloric acid (HCl), another component of the gastric juice, plays a crucial role in creating the pH required for pepsin activity. Parietal cells produce HCl by secreting hydrogen and chloride ions. When pepsinogen and hydrochloric acid exist together in the gastric juice, pepsin takes its active form. Through the actions of pepsin and the squeezing properties of the stomach, the food bolus enters the intestines as a liquidy mixture of partially digested food particles, called chyme.

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Issues of Concern

Pepsin depends on an acidic environment for protein digestion. Therefore, it is most effective at a pH of approximately 1.5 to 2. Low pH allows pepsinogen to cleave itself and form active pepsin. When it reaches the duodenum, though, it assumes an inactive form as the pH rises above 6. Nonetheless, protein digestion continues to take place throughout the small intestines via the effects of pancreatic enzymes: trypsin, chymotrypsin, elastase, and carboxypeptidase. As such, pepsin is not essential for life, and protein digestion can still take place in the absence of pepsin. It is worth mentioning that pepsin remains structurally stable until at least a pH of 8. Therefore, it can always be reactivated as long as pH remains below 8. This characteristic proves relevant in the pathophysiology of laryngopharyngeal reflux, as discussed later in the article.[1]

As mentioned earlier, the stomach provides pepsin with an ideal environment for protein digestion. Doing so helps with breaking down proteins into smaller nutrients, but at the same time, puts the stomach at risk of autodigestion. Therefore, a protective mechanism should exist to help maintain mucosal integrity. Fortunately, a mucus lining loaded with bicarbonate molecules helps protect against hydrochloric acid and creates a near-neutral pH environment that deactivates pepsin.[2]

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Function

Pepsin is an endopeptidase that breaks down dietary proteins reaching the stomach into amino acids. It functions by digesting peptide bonds, the predominant chemical bonds found in proteins. In response to various stimuli, small basophilic cells in the deeper layers of gastric glands, known as Chief cells, produce pepsinogen. Notably, acetylcholine, gastrin, and low pH directly stimulate chief cells to secrete pepsinogen. Acetylcholine is a neurotransmitter released from vagal parasympathetic nerve terminals in the "cephalic phase" of food digestion. Besides enhancing chief cell activity, it also stimulates parietal cells to produce hydrochloric acid (HCl) via their proton pumps. The low pH imposed by HCl breaks down pepsinogen into its active form, pepsin. Gastrin is another gastrointestinal hormone released by G cells in the stomach antrum and the duodenum. G cells secrete gastrin in response to many stimuli, including stomach distension, amino acids and peptides, high pH, and vagal stimulation. Similar to acetylcholine, gastrin also activates parietal cells to secrete hydrochloric acid (HCL) on top of its chief cell stimulatory effects. It does so both directly, and indirectly, through the action of histamine released by enterochromaffin-like (ECL) cells. Histamine is, in fact, the most potent activator of parietal cells. Somatostatin, on the other hand, is an inhibitory gastrointestinal hormone released by D cells in the duodenum and stomach antrum. It inhibits pepsinogen release from chief cells, thereby opposing the effects of gastrin, HCl, and acetylcholine.[3]

Source : www.ncbi.nlm.nih.gov