Lecture 22: Salivary + Pancreatic Secretion Flashcards
(24 cards)
Salivary glands
Parotid, sublingual, submandibular
Functions of saliva
- Hydration for mastication/deglutition
- Bicarb secretion
- Produce R factor for Vit. B12
- Protect vs bacteria w/ lysozyme, buffers, IgA
- Initiate food digestion (lingual amylase, lipase)
Salivary α-amylase (ptayalin)
Cleaves α-1,4 glycosidic bonds in interior of molecules, optimal pH = 6.7
Cells involved in salivary secretion
Initial saliva secreted by acinar cells (myoepithelial cells squeeze out); ductal cells modify
Salivary acinar cell secretion method
H2O + Na+ follow Cl- into lumen. K+ leak drives Na+/K+ exchanger, Cl- import
Saliva modification by ductal cells mechanism
Active Na+, Cl- absorption; K+, bicarb secretion. Duct is H2O impermeable; saliva becomes hypotonic
Flow rate effect on ionic saliva composition
Concentration modification depends on time saliva contacts ductal cells; more contact time -> more hypotonic
Exception to flow rate effect on saliva
Bicarb; bicarb secretion selectively stimulated when saliva production is (both symp. + parasymp.)
Regulation of saliva secretion
Saliva secretion exclusively under ANS neural control (symp. + parasymp., parasymp. dominates)
What does neural stimulation of the salivary glands do?
Stimulation increases blood flow to salivary glands e.g. bradykinin vasodilation.
Increase in cap. P -> more H2O/electrolyte filtration -> more saliva
Pancreatic secretion phases
- Cephalic
- Gastric
- Intestinal
Cephalic phase pancreatic secretion
Vagal efferent stim. -> some enzyme/bicarb secretion
Vagal stim. -> minor gastrin secretion -> pancreatic secretion augment.
Intestinal phase pancreatic secretion
AAs/peptides/FAs/duodenal acid load stim. vaso-vagal reflex, CCK/secretin release -> huge increase in enzyme/bicarb secretion
CCK stimulation of pancreas
Direct: stim. enzyme/bicarb secretion
Indirect: stim. vaso-vagal reflex -> more pancreatic secretion
CCK potentiates ductal cell secretion
I cells
Secrete CCK in response to AAs/small peptides/FAs in intestine; acinar cell stim. via IP3/Ca2+ for enzymes
S cells
Secrete secretin in response to intestinal acid; ductal cell stim. via cAMP for aqueous bicarb secretion (Na+, bicarb)
Intestinal phase pancreatic secretion synergy
ACh, CCK, secretin have synergy and potentiate each other to increase pancreatic enzyme/bicarb output
Pancreatic duct cell secretion mechanism
- Bicarb is both imported and produced
- Acid tide
- CFTR; Na+, H2O follow Cl-
- CFTR countered by bicarb secretion
Flow rate effect on pancreatic juice composition
Low Q: pancreas juice has more Na+, Cl-
Higher Q: pancreas juice has more Na+, bicarb e.g. secretin stimulation
Pancreatic proteases
Produced and secreted as zymogens
Pancreatic Secretory Trypsin Inhibitory
Further protects pancreas from autodigestion
Activating enterokinase
Found on enterocyte brush border to activate trypsinogen; anatomically separate from secretion site
Acinar pancreatic enzyme synthesis process
1/2. RER synthesis
3. Proteins sorted to Golgi
4. Secretory/condensing vacuole packaging
5. Zymogen concentration in granules w/ PSTI
6. Secretory stimulation causes zymogen granules to fuse w/ membrane
Acute pancreatitis
Causes: ischemia, obstruction, alcohol leading to premature zymogen activation
Induces acinar necrosis/autodigestion; proteases escape to EC space and cause inflammation