Regulation of gastrointestinal tract functions
Regulation of the GIT functions is mediated by:
a.Nervous regulation
b.Hormonal regulation
a. Nervous regulation
This is done by extrinsic innervation (autonomic nervous system) and intrinsic
innervation (enteric nervous system).
Electrical activity of gastrointestinal smooth muscle:
-Normally, the resting membrane potential (RMP) of gastrointestinal smooth
muscle is about -55 mV (-50 to -60 mV).
-The gastrointestinal smooth muscles show rhythmic changes (continuous
slow electrical activity) in the membrane potential called slow waves or basal
electrical rhythm (BER).i.e unstable RMP.
-Once threshold potential is reached, there is initiation of action potential
(spike potential) resulting in complete muscle contraction.
Electrical activity of gastrointestinal smooth muscle
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1. Slow wave potential 2. Spike potentials
Basic electrical rhythm (BER)
They are spontaneous slow undulating Consists of depolarization and
changes in the RMP between 5 – 15 repolarization wave i.e. true
mV i.e. not true action potentials. action potential occurring
automatically (spontaneous
Initiated by interstitial cells of Cajal
action potential).
(pacemaker cells).
Composed of gradual depolarization,
followed by gradual repolarization.
The cause is unknown but may due to Depolarization is due to slow
change in the activity of Na+-K+ pump. entry of large amount of Ca++
They don’t cause Ca++ entry or through Ca++ channels. This
activation of smooth muscle. calcium is important for its
contraction. Repolarization is
due to K+ efflux.
Control the intermittent appearance of Cause muscle contraction.
spike potentials at the peak of slow
waves when the RMP changes from
(– 60 to – 40 mV) (threshold). They do
not directly cause muscle contraction
Their frequency are about 3/min in the
body of stomach, 9/min in the terminal
ileum.
Rate of muscle contraction in each
organ depends on the inherent rate of
BER.
Interstitial cells of Cajal (pace maker) are non-contractile cells located
between the circular and longitudinal muscle layers.
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Functional syncytium of the GIT smooth muscle:
-Sheets of smooth muscle cells are connected by gap junctions, which serve
as points of low electrical resistance (permit movement of ions between
adjacent cells).
-Through gap junctions, action potentials in pace maker cells spread rapidly to
all smooth muscle cells. So the whole muscle sheet contracts as a unit i.e
(functional syncytium)
Syncytium of the GIT smooth muscle
Excitability is increased (RMP becomes less –ve or more depolarized) by
the following conditions:
(1) Stretch of the muscle.
(2) Parasympathetic stimulation.
(3) Stimulation with acetylcholine.
(4) Certain GIT hormones as gastrin and cholecystokinin (CCK).
These factors cause the starting point of the slow wave potentials to come
nearer to the threshold level→ peak of slow wave potential reaches
threshold→ action potentials at the peak followed by muscle contraction.
Excitability is decreased (RMP becomes more –ve or hyperpolarized) by:
(1) Catecholamines.
(2) Sympathetic stimulation.
(3) Certain GIT hormones as secretin and gastric inhibitory peptide (GIP).
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These factors cause the starting point of the slow wave potentials to come
away from the threshold level→ peak of slow wave potential doesn’t reach
threshold→ no action potentials → no muscle contraction.
Innervation of the gastrointestinal system (GIT):
a.Autonomic nervous system:
(1) Parasympathetic supply:
-It is transmitted mainly through the vagus nerve which arises from dorsal
vagal nucleus in the medulla oblongata to supply the esophagus, stomach,
small intestine, proximal part of large intestine (ascending colon) and
pancreas.
-Sacral parasympathetic supply (pelvic nerve) arises from the middle 3 sacral
segments (S2, 3 and 4) to supply the rest of the colon, rectum and anal canal.
-The preganglionic fibers entirely terminate on local nerve plexuses; myentric
and submucosal.
-Parasympathetic stimulation is generally stimulatory (increasing the activity of
enteric nervous system) i.e. increasing the secretory and motor function of
GIT and causes relaxation of their sphincters.
(2) Sympathetic supply:
- Arises from LHC of T5 to L2 segments as preganglionic fibers and relay in
prevertebral (collateral) ganglia as celiac and mesenteric ganglia. The
postganglionic fibers reach the GIT through greater and lesser splanchnic
nerves.
-Most of the sympathetic fibers terminate on local nerve plexuses.
-Sympathetic stimulation is generally inhibitory decreasing the secretory and
motor function of GIT and causes contraction of their sphincters.
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Extrinsic innervation of GIT
b.Enteric nervous system (ENS; local nerve plexus):
-The GIT has its own intrinsic nervous system that begins in the esophagus
and extends down to the anus.
-Includes myentric (Auerbach's) plexus which regulates GIT motility and
submucosal (Meissener’s) plexus which regulates GIT secretion, blood flow
and many sensory functions.
-Each plexus is composed of large number of neurons connected by
interneurons. Their dendrites end on receptors in the GIT wall and their axons
terminate around smooth muscle or glands of GIT (exocrine or endocrine
glands).
-Stimulation of myentric plexus leads to increased motor activity of the gut by
increased tonic contractions, the rate and intensity of the rhythmic
contractions and velocity of conduction of excitatory waves. However, some
myentric plexus fibers are inhibitory and secrete inhibitory transmitter
vasoactive intestinal peptide (VIP).
-The neurons of the enteric nervous system release many substances as
acetyl choline, gastrin releasing peptide (GRP), substance P, vasoactive
intestinal polypeptide (VIP), serotonin,…………..
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-The parasympathetic and sympathetic nervous signals to the GIT can
strongly alter the degree of activity of the ENS.
Enteric nervous system
Reflexes for nervous regulation of GIT:
1.Localized, short reflexes:
-Occur entirely within the enteric nervous system to control the gastric motility
(peristaltic and mixing movements) and secretion.
-The receptor presents in the wall of the gut and it is stimulated by either
stretching of the wall or intramural stimuli (digestive products, acid or osmotic
pressure).
-The afferent is the dendrites of the neuron of the enteric plexus.
-The center the cell body of the neuron of the enteric plexus.
-The efferent is the axon of the neuron of the enteric plexus.
-The effector organ is either the smooth muscles or glands of GIT.
-The response is controlling GIT motility or secretion.
2.Ganglionic reflexes: They start from receptor presents in the wall of the gut
to reach the prevertebral sympathetic ganglia (which act as center) and then
back to GIT e.g.
- Enterogastric reflex: distension of duodenum, increased acidity or
presence of fat in duodenum → reflex in gastric emptying.
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- Gastrocolic reflex: distension of stomach or duodenum → mass
contraction in a wide spread area of the colon (mass peristalsis or peristalsis
rush) to deliver stool to the sigmoid colon.
- Gastroileal reflex: distension of stomach or duodenum → reflex
relaxation of ileocaecal sphincter.
- Colonoileal reflex: distension of caecum → reflex contraction of
ileocaecal sphincter.
3. Central (long) reflexes: They start from receptor in the gut to CNS
(cerebral cortex, spinal cord or brain stem) then back to GIT. They include
reflexes controlling GIT motility and secretion (unconditioned and conditioned
reflexes), pain reflexes or defecation reflexes.
Unconditioned (inborn) Conditioned (acquired)
reflex reflex
Need for Does not need cerebral Needs cerebral cortex and
cerebral cortex cortex or training. training.
or training
Stimulus Mechanical or chemical Seeing, smelling, hearing
stimuli due to presence or even thinking of food.
of food in GIT or by
digestive products.
Receptor In the mouth or wall of Visual, smell or auditory
GIT. receptors (special sense).
Afferent Facial, glossopharyngeal Optic, olfactory or
or vagus n. cochlear nerves.
Center Vagal nucleus in Cerebral cortex.
medulla oblongata.
Efferent Vagus nerve. Vagus nerve.
Effector organ GIT GIT
Response GIT motility and GIT motility and
secretion secretion
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b.Hormonal (chemical) regulation
-Gastrointestinal motility and secretion are controlled by a great number of
GIT hormones which polypeptides secreted by special mucosal cells in the
GIT are called enteroendocrine cells or APUD cells (amine precursor uptake
and decarboxylation).
-They are classified into:
- Gastrin family: Gastrin and cholycystokinin (CCK).
- Secretin family: Secretin, gastric inhibitory peptide (GIP) and vasoactive
intestinal peptide (VIP).
- Other hormones: Motilin and Somatostatin.
GIT hormonal regulation
A) Gastrin:-
-It exists in 3 forms according to the number of A.A (G14, G17 and G34).
-It is secreted by G cells in the stomach and duodenum.
-Its secretion is stimulated by:
Luminal factors: Including gastric distension decreased gastric acidity (PH
> 2) and presence of protein digestive products in the stomach.
Vagal stimulation (chemical transmitter is gastrin releasing peptide).
Actions:
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-Stimulation of gastric motility and secretion especially HCl (main action).
-Helps normal growth of gastrointestinal mucosa (main action).
-Stimulation of small intestinal motility.
-Contraction of lower esophageal sphincter preventing reflux of gastric
contents into the esophagus.
-Relaxation of ileocecal sphincter.
-Stimulation of insulin and glucagon secretion (only in large doses).
Feedback control (-ve feedback): Gastrin → HCl → gastrin.
B) Cholecystokinine (CCK):-
-It is a polypeptide hormone containing 33 amino acids.
-It is secreted by I cells in the duodenal and jejunal mucosa.
-Its secretion is stimulated by:
-Protein digestive products particularly peptides and amino acids.
-Long chain fatty acids.
-Actions:
- Stimulation of enzymatic pancreatic secretion (small in volume, poor in
HCO3- and rich in enzymes).
- Contraction of gall bladder and relaxation of the sphincter of Oddi
which causes evacuation of the gall bladder.
- Augmenting the action of secretin.
- Inhibition of gastric emptying and secretion.
- Contraction of pyloric sphincter.
- Stimulation of intestinal motility.
- Stimulate insulin secretion.
Feedback control (+ve feedback control): Products of digestion→CCK →
bile and pancreatic secretion → digestive products → CCK.
C) Secretin:-
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-It exists in only one form containing 27 amino acids.
-It is secreted by S cells in the duodenal and jejunal mucosa.
-Its secretion is stimulated by:
Arrival of acid chyme with PH < 4.5 to the duodenum.
Protein digestive products and Fatty acids.
Actions:
- Stimulation of aqueous pancreatic secretion (large in volume, rich in
HCO3- and poor in enzymes).
- Augmenting the action of CCK.
- Inhibition of gastric motility and secretion.
- Contraction of pyloric sphincter.
Feedback control (-ve feedback): Duodenal acidity → secretin →
secretion of alkaline pancreatic secretion→ acidity → secretin.
D) Gastric inhibitory peptide (GIP):-
-It is secreted by K cells in the mucosa of the duodenum and jejunum in
response to presence of fat and to lesser extent carbohydrates.
-Actions: It decreases the gastric emptying into the duodenum, when the
upper small intestine is over supplied with food products and stimulate insulin
secretion.
E) Vasoactive intestinal peptide (VIP):-
-It is secreted from upper part of small intestine in response to products of
digestion.
Actions:
- V.D of intestinal blood vessels.
- Inhibition of gastric secretion.
- Stimulation of excessive intestinal secretion rich in electrolytes and
water.
- Relaxation of GIT smooth muscle.
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F) Motilin:
-It is secreted by special cells scattered in the small intestine in response to
the products of food digestion.
Actions: Major regulator of the migrating motor complex (MMC) that controls
gastrointestinal motility between meals.
G) Somatostatin:
It is secreted from the stomach and upper part of the small intestine.
Actions: -Inhibits gastric secretion and motility.
- Inhibits secretion of: gastrin, secretin, GIP, VIP and motilin.
- Inhibits pancreatic exocrine secretion and gall bladder contraction.
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