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1 - GI control mechanisms


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What are the two basic structural subdivisions found throughout the GI tract? What are the functions of each?
*mucosal layer: absorption and secretion
*muscular layer: movement of contents
What are the two layers of the muscular layer? What action does each have on the size of the GI tract?
*outer longitudinal layer - shortens the length of the tube
*inner circular layer - constricts the diameter of the lumen
What is the primary blood supply of the GI system? What percentage of cardiac output is consummed by the GI tract during a meal? During flight-or-fight?
*splanchnic circulation
*65% during a meal; 0% during flight-or-fight
What is the role of parasympathetic innervation in control of GI function? Sympathetic innervation? How is different from the innervation of the CV system?
*parasympathetic is stimulatory
*sympathetic is inhibitory
*this is the opposite of innervation of the CV system
Describe the effect of parasympathetic and sympathetic innervation of motility, secretion, and sphincter and vasculature tone in the GI tract.
*parasympathetic innervation increases motility, increases secretion, relaxes sphincters, and dilates vasculature
*sympathetic inervation has the opposite effects
What are two reflexes controlled by motor programs.
The swallowing and peristaltic reflexes.
Where are the myenteric and submucosal plexuses located?
The myenteric plexus is between the layers of the muscular layer and the submucosal plexus is found between the submucosa and the inner muscular layer.
The movement of what ion controls the contraction of smooth muscle cells in the GI system?
What are interstitial cells of Cajal? What is their function?
They are the pacemaker cells of the GI tract that resemble a cross between a smooth muscle cell and a fibroblast. They generate driving potentials which stimulate slow wave potentials in smooth muscle cells.
How are ICC connected to smooth muscle cells?
Through gap junctions.
How do GI smooth muscle cells repolarize (i.e. return to RMP)?
Ca++ stimulates K+ channels to open which allows an efflux of this ion and repolarization of the cell.
Is the rate of basal oscillation of GI smooth muscle cells constant throughout the tract? Why or why not?
It is not - there is a gradient from 14/min in the duodenum to 7/min in the ileum. It is thought that this gradient propels lumenal contents in one direction.
What is the action of ACh on smooth muscle cells?
*it depolarizes them, bringing them above threshold potential and allowing voltage-gated Ca++ channels to open and cause "fast" action potentials
*inhibits K+ channels to prevent repolarization
*stimulates synthesis of IP3
What is the action of VIP on smooth muscle cells?
*hyperpolarizes cell
*activates K+ channels which induces repolarization
*induces cAMP production which lowers [Ca++]
*decreases pacemaker frequency
What initiates the peristaltic reflex?
Food in the lumen stimulates mechanoreceptors which release serotonin, which in turn stimulates interneurons in the submucosal plexus.
What are the end actions of the peristaltic reflex?
*mucus release is stimulated in front of the bolus
*ACh stimulates muscular contraction behind the bolus
*VIP and NO induce muscular relaxation in front of the bolus
Describe the smooth muscle action seen in W/Wv mice.
These mice lack ICC and their smooth muscle cells show erratic Ca++ dependent potentials. There are random contractions, but no organized waves. As a result, food moves much more slowly.
What type of symptoms are seen in humans who have defective ICC or lack them altogether?
Low motility resulting in constipative disease.
What are two specific mechanisms of mucosal immunity in the GI tract?
*M cells pick up and present antigen
*production of secretory IgA by B-cells
How is the pacemaking seen in the GI system different from that of the cardiovascular system?
In the cardiovascular system, pacemaking is focal, rapid, and nearly synchronous. In the gut it is distributed, slow, and variable in time and space.
Are driver potentials produced by ICC due to the movement of Ca++, Na+, or K+?
They are initiated by the opening of a channel that doesn't discriminate between Na+ or K+. Ca++ does not seem to be involved as the cells continue to generate potentials even when a Ca++ channel blocker is applied.
How do excitatory motor neurons in the myenteric plexus stimulate smooth muscle cells of the muscular layer?
They release ACh which has a variety of stimulatory effects on the smooth muscle cells.
How do signals from excitatory motor neurons affect the slow wave potentials generated by smooth muscle cells in the gut?
They increase the amplitude and duration of the slow wave potentials which causes the muscle to contract rhythmically. Also, ACh allows the generation of fast potentials.
How do inhibitory motor neurons affect the slow wave potentials of smooth muscle cells in the gut?
They decrease the amplitude, duration, and frequency of the slow wave potentials which causes the muscle to relax.
How do inhibitory motor neurons exert their effect on smooth muscle cells?
They release VIP which has a variety of inhibitory effects.

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