Salivary secretions (Choudhury lecture) Flashcards
Saliva functions
Taste Lubrication Protection Digestion Speech Not essential for life
Salivary control
Saliva is under
neuronal control
not hormonal
(hormones modify)
Salivary glands
Salivary glands: (ectodermal)
Submandibular: serous/mucous 70% (thick saliva)
Sublingual: serous/mucous 5% (thick saliva)
Parotid (largest): serous 25% (thin saliva, no mucin)
Smaller glands: mucous
Constituents of saliva and their functions
Water facilitates speech, dissolving, tasting food, swallowing
Mucus lubrications, food into cohesive bolus
a-amylase (ptyalin) carbohydrate digestion, cleaves a-1,4 glycosidic bonds in starch (not essential)
Lingual lipase lipid digestion (milk-fats), hydrolysis of dietary lipid (not essential)
Ribonuclease RNA digestion (not essential)
Lysozyme antibacterial (bacillus & streptococcus), innate and acquired immunity
Lactoferrin chelates iron (inhibits microbial growth)
Lactoperoxidase antibacterial (kills bacteria in milk and mucosal lining)
Glycoprotein of IgA secretory IgA-immunologically active against virus and bacteria
EGF, NGF mucosal growth and protection
Kallikrein activates bradykinin – dilates arterioles, constricts veins increase blood
flow to secretory glands
Bicarbonate minimizes tooth decay (neutralizes bacterial acid)
(HCO3-) neutralizes refluxed gastric acid into lower esophagus (heartburn)
Hypotonic taste (can taste carbohydrates, fats and not protein –tofu!) Low osmolality
Two types of salivary glands
- serous (parotid- secretes non-viscous saliva composed of water, electrolytes and enzymes)
- mixed (submandibular, sublingual- secretes viscous saliva rich in mucin glycoproteins)
Salivary gland acini
primary secretion-saliva, plasma (H2O, Na+, Cl-, K+, HCO3-, amylase)
myopepithelial cells
motile, contracts, expels saliva
salivary gland ductal cells
modifies secretion by modifying electrolytes, Na+, Cl- reabsorbed K+, HCO3- secreted
- **Ductal cells are water impermeable, water is not absorbed along with the solute, water remains in lumen and saliva is secreted hypotonic relative to plasma
- **
Striated duct epithelium tight junction
H2O cannot leave duct
The story of salivary ions
Initial saliva is produced by acinar cells
Subsequently modified by ductal epithelial cells
Salivary ducts are impermeable to water and sodium is continually reabsorbed
Lumen of ductal cells contains
3 transporters:
- Na +- H + exchange,
- Cl - HCO 3 exchange, and
- H +- K + exchange
Basolateral membrane contains:
- Na +/K + ATPase and Cl channels
Net absorption of Na + & Cl causes
NaCl in saliva lower than in plasma
Net secretion of K + and HCO 3 causes
K + and HCO 3 in saliva higher than in
plasma
Changes in ionic composition of saliva
Ionic composition of saliva changes as salivary flow rate changes
Duct cells modifies the composition of saliva
At highest flow rates (4 mL/min), final saliva resembles plasma (high Na+, Cl-, low K+)
as the ductal cells have less time to modify the saliva
At lowest flow rates (
The short story on neuronal regulation of saliva
Both Symp and Parasymp stimulates secretion
Parasymp stimulates more than Symp
Parasymp: major M3 receptors, increase secretion of watery saliva
Symp: major b receptors, increase viscous saliva, minor a receptors – watery saliva
The long story on regulation of saliva
Salivary acinar & ductal cells have both Symp and
Parasymp innervation
Neuronal: ANS (symp & parasymp) stimulate &
regulate the flow of salivary gland secretions
Symp NS stimulates secretion:
- increases cAMP (major), increase amylase secretion
- increases IP3 (minor), increase fluid secretion
Parasymp NS stimulate secretion -Dominant
- increases IP3 (major), increase fluid secretion
- vasodilation to surrounding blood vessels
- activation of both acinar & duct cells transporter
- releases kallikrein
- greater influence than Symp NS
Hormonal:
- ADH (antidiuretic hormone) &
- Aldosterone modify composition of saliva Na +, K +
- Kallikrein produces bradykinin (potent vasodilator),
increases blood flow and increase salivary secretions
Salivary regulation compared to rest of GI tract
Salivary secretion and composition are controlled solely by the autonomic nervous system, in contrast, other parts of the GI tract include local reflexes and hormonal mechanisms as well
Stimulation and inhibition of saliva
CNS and its ANS respond to external
events and either stimulate or inhibit
activities of salivary glands
Stimulated by:
smell, taste, sound, sight, chewing,
spicy or sour tasting foods, smoking,
nausea, vomiting, sympathomimetic
(ephinephrine), parasympathomimetics
(acetylcholine, pilocarpine, muscarine),
histamine, etc.
Inhibited by:
sleep, fear, shock, anti depressants,
fever, dehydration, fatigue,
antihistamines, anti-parkinson drugs,
anti-muscarinic drugs, marijuana
(anti-cholinergics lead to dry mouth)
monoamine oxidase inhibitors, etc.
Oxyntic glands
are located in the fundus and body/corpus of stomach, contain three types of cells.
What cells secrete what in oxyntic glands?
- The parietal (oxyntic) cells secrete
- HCl (protein breakdown, pepsinogen activation, kills most microbes)
- intrinsic factor (IF) (necessary for the absorption of vit. B12 by the ileum)
2. Peptic (chief, zymogenic) cells secrete – Pepsinogen/zymogens – converted to pepsin
3. Mucous cells secrete - Mucus (thick/thin mucous)
Pyloric glands
are located in the antrum & pyloric regions of stomach, contain G & some mucous cells.
What cells secrete what in pyloric glands?
- G cells secrete - Gastrin (hormone) – stimulates parietal cells (HCl) & peptic cells (pepsinogen)
2. Mucous cells secrete - Mucous (thick/thin mucous)
gastric secretion –> Inverse relationship between…
luminal conc of
H+ and Na+
Direct stimulation of parietal cell
-ACh released from vagus nerve binds to M3 receptors
-Histamine released from ECL cell binds to H2 receptors
-Gastrin released from G cell binds to CCKB receptors
-All three agonists synergistically stimulate and
potentiate acid secretion from parietal cell
Indirect stimulation of parietal cell
-ACh released from vagus nerve binds to M3
receptors on ECL cell and release histamine
-Gastrin released from G cells binds to CCKB
receptors on ECL cell to release histamine
-Histamine released from ECL cell (by action of
ACh & gastrin) binds to H2 receptors on
parietal cell
potency of gastrin vs. histamine
Agonists: ACh, Gastrin and Histamine
all stimulate parietal cell to secrete acid
ACh binds to M3 receptors
Gastrin binds to CCKB receptors
(gastrin 1500 X potent than histamine in releasing HCl)
Histamine binds to H2 receptors
Parietal cell inhibitors
Somatostatin and PGs directly binds to parietal cell and inhibits Histamine Somatostatin binds to SST receptors PGs binds to PGs receptors Both are linked to G protein (Gai) and oppose action of histamine and Gs
Absence of IF and Vit B12 results in …
Pernicious anemia, neurological disturbances
(numbness in extremities and weakness)
Vitamin B12 deficiency is caused by…
Decreased dietary intake (vegan)
Decreased absorption
- gastric resection
(decreased IF)
- autoimmune disease
(antibody against parietal
cells and IF)
All leads to decrease Vit B12
level and prenicious anemia
This produces macrocytic anemia (megablastic anemia) as B12 is required for DNA synthesis in RBC progenitor cell in bone marrow
Prolong B12 deficiency causes
neurological symptoms
agents causing mucosal damage
H. Pylori ( > 80%)
Zollinger-Ellison syndrome, tumor
that causes excessive secretion of
gastrin, which stimulates acid
hyper-secretion.
NSAIDS (aspirin) inhibits COX-1
- COX-1 forms PGs
- PGs protects gastric mucosa
Alcohol
Bile acids
Stressful situations
- physical
- emotionalgastric acid determination
Serum gastrin levels and gastric acid secretion used to evaluate gastric function
Pentagastrin is used to stimulate acid secretion
histamine receptor antagonists
cemetidine, rantidine
muscarinic antagonist
dycyclomine
proton pump inhibitor
omeprazole
