Salivary secretion Flashcards
Name and describe cells involved in salivary secretion
Serous cells: These are responsible for secreting watery, enzyme-rich saliva. They contain granules that are filled with digestive enzymes such as amylase, which helps break down carbohydrates.
Mucous cells: These cells produce a thicker, more viscous saliva. They contain large amounts of glycoproteins called mucins, which help to lubricate and protect the oral cavity.
Myoepithelial cells: These cells are located around the acini (clusters of secretory cells) and ducts of the salivary glands. They have contractile properties and help to move the saliva through the ducts and into the oral cavity.
Describe the composition of salivary secretion
Water: Saliva is mostly composed of water, accounting for about 99% of its volume. Water serves to moisten and lubricate the mouth and facilitates the mixing and breakdown of food particles.
Electrolytes: Saliva contains various electrolytes such as sodium, potassium, chloride, bicarbonate, and phosphate ions. These ions help maintain the pH balance of the mouth and aid in the digestion of food.
Enzymes: Saliva contains several enzymes, including amylase, which breaks down carbohydrates, lipase, which breaks down fats, and protease, which breaks down proteins. These enzymes begin the process of digestion before food enters the stomach.
Mucus: Saliva contains mucus, which helps to lubricate and protect the lining of the mouth and throat.
Antibodies: Saliva contains immunoglobulin A (IgA), which helps to defend against bacteria and viruses that enter the mouth.
Growth Factors: Saliva also contains growth factors, such as epidermal growth factor (EGF) and nerve growth factor (NGF), which help to stimulate the growth and repair of tissues in the mouth.
Describe the mechanisms involved in generating a hypotonic saliva
- Secretion of na+ and cl- into glandular ducts.
- Aldosterone stimulates secretion of Na+ and ACH stimulates secretion of NA+ and cl-
- This creates an osmotic gradient which draws water from intestinal space into the ducts creating hypotonic salivia
- Reabsorption of K+ can increase hypotonicity across the ductal epithelium
The primary mechanism for generating hypotonic saliva is the active secretion of electrolytes, primarily sodium and chloride ions, into the lumen of the glandular ducts. This creates an osmotic gradient that draws water from the interstitial space into the ducts, resulting in the production of a hypotonic saliva.
The secretion of electrolytes is controlled by the secretory cells of the salivary glands, which are specialized epithelial cells that line the ducts. These cells actively transport ions across their membranes, using ATP-dependent ion pumps and ion channels.
The transport of ions is regulated by several factors, including hormones such as aldosterone and vasopressin, and neurotransmitters such as acetylcholine and adrenaline. These molecules bind to specific receptors on the surface of the secretory cells, activating various intracellular signaling pathways that modulate ion transport.
In addition to the active secretion of electrolytes, the reabsorption of solutes such as potassium ions can also contribute to the hypotonicity of saliva. This occurs across the ductal epithelium and helps to maintain the ionic balance in the saliva.
Describe neural regulation of salivary secretion
- Parasympethetic nervous system releases ACH, which binds to muscarinic receptors on saliviary gland cells, increasing intracellular calcium levels and activating other pathways
- This activates ion channels and pumps, resulting in the secretion of salivia.
- Parasympathetic stimulation promotes vasodilation which increases blood flow to the saliviary glands promoting secretion
- Sympathetic NS inhibits salivia secretion
- Norepinephrine is released which binds to alpha – adrenergic receptors on salivary gland cells, decreasing intracellular calcium levels and inhibits signalling pathways
- Less secretion of salivia, and increased vasoconstriction inhibits production
explain the mechanism for gastric acid secretion
The hypothalamus receives input from the limbic system, which can modulate gastric acid secretion through emotional and stress-related responses. The medulla oblongata, on the other hand, is involved in the regulation of gastric acid secretion via the vagus nerve.
The peripheral nervous system also plays a key role in regulating gastric acid secretion. The vagus nerve, which is the main parasympathetic nerve that innervates the stomach, stimulates acid secretion through the release of acetylcholine. In contrast, sympathetic nerves that innervate the stomach inhibit acid secretion through the release of norepinephrine.
The hormone gastrin, which is produced by the G cells in the stomach, stimulates acid secretion by activating the H+/K+-ATPase pump in the parietal cells. Other hormones such as histamine, somatostatin, and prostaglandins also regulate gastric acid secretion by modulating the activity of the H+/K+-ATPase pump or the parietal cells directly.
1.The parietal cell is activated by various stimuli, including acetylcholine, gastrin, and histamine.
- Once activated, the parietal cell pumps hydrogen ions (H+) into the stomach lumen, using an enzyme called H+/K+-ATPase, or the proton pump. This proton pump is located in the apical membrane of the parietal cell.
- At the same time, chloride ions (Cl-) are secreted into the lumen of the stomach through the Cl^-/HCO3^- exchanger, which is also located in the apical membrane of the parietal cell.
- Hydrogen and chloride ions combine in the lumen of the stomach to form hydrochloric acid (HCl), which has a pH of about 1.5-2.0.
- The secretion of gastric acid by the parietal cell is balanced by the secretion of bicarbonate (HCO3^-) by the epithelial cells lining the gastric glands, which helps to neutralize any acid that may leak back into the gastric mucosa.
- The production of gastric acid by the parietal cell is also regulated by negative feedback mechanisms to prevent overproduction of acid. For example, high levels of acid in the stomach can stimulate the release of somatostatin, which inhibits the secretion of gastric acid.
Describe the cephalic, gastric and intestinal influences on gastric acid secretion
Cephalic phase: This phase is triggered by the sight, smell, taste, or thought of food, and it involves the activation of the vagus nerve, which releases acetylcholine. This, in turn, stimulates the secretion of gastrin-releasing peptide (GRP) and gastrin from the G cells in the antrum of the stomach. Gastrin then binds to the parietal cells in the stomach lining, promoting the secretion of gastric acid.
Gastric phase: Once food enters the stomach, the stretch receptors in the stomach wall are activated, which triggers the release of gastrin from the G cells. Gastrin stimulates the parietal cells to secrete more acid, and it also increases the tone of the lower esophageal sphincter (LES) to prevent reflux.
Intestinal phase: As food moves into the small intestine, it stimulates the release of hormones such as secretin and cholecystokinin (CCK) from the duodenal mucosa. These hormones inhibit the secretion of gastric acid by reducing the release of gastrin and stimulating the secretion of bicarbonate-rich pancreatic juice, which neutralizes the acid in the duodenum.
Describe the mechanisms regulating pancreatic secretion: name the exocrine
secretions of the pancreas Describe the factors which cause release of secretin
and cholecystokinin and how these intestinal hormones modify the composition
of pancreatic juice
Secretin is released in response to the presence of acidic chyme in the duodenum, which is the first segment of the small intestine. The acidic chyme stimulates the S cells in the duodenal mucosa to release secretin into the bloodstream. Secretin then travels to the pancreas and stimulates the secretion of bicarbonate ions from the pancreatic duct cells, which helps to neutralize the acidic chyme as it enters the duodenum.
CCK is released in response to the presence of fats and proteins in the chyme. The fats and proteins stimulate the I cells in the duodenal mucosa to release CCK into the bloodstream. CCK then travels to the pancreas and stimulates the secretion of digestive enzymes from the acinar cells of the pancreas, as well as the contraction of the gallbladder to release bile into the duodenum.
Secretin stimulates the secretion of bicarbonate ions from the duct cells of the pancreas. Bicarbonate ions help to neutralize the acidic chyme as it enters the duodenum, creating a more favorable pH environment for digestive enzymes. Secretin also stimulates the production of water and electrolytes, which help to increase the volume of pancreatic juice.
CCK, on the other hand, stimulates the secretion of digestive enzymes from the acinar cells of the pancreas, including enzymes such as pancreatic lipase, amylase, and proteases. These enzymes help to break down fats, carbohydrates, and proteins in the chyme, allowing for better absorption and digestion in the small intestine. CCK also stimulates the contraction of the gallbladder to release bile into the duodenum, which aids in the digestion and absorption of fats.
