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Control of the gastrointestinal tract (sympathetic and

parasympathetic)
Sympathetic and Parasympathetic divisions typically function in opposition
to each other. The gastrointestinal tract is regulated, in part, by the
autonomic nervous system.
This highly sophisticated regulatory system requires coordination of
motor, secretory, digestive and absorptive function.
Parasympathetic supply:
Parasympathetic nerves that supply the oesophagus, stomach, small
intestine, ascending colon, liver, gall bladder and pancrease arise from the
medulla and conducted through the vagus nerve.
Parasympathetic nerves to the rest of the colon arise in sacral spinal
cord and conducted through the pelvic nerves.
In general stimulatory
Sympathetic Supply:
Arise in the spinal cord
Postganglionic fibres from the prevertebral ganglia innervate the GI
tract
In general inhibitory
The sympathetic, parasympathetic, and ENS divisions of the autonomic
nervous system (ANS) innervate the digestive tract. Neural control of the
gut is hierarchical, with five basic levels of integrative organization Level 1
is the ENS, which behaves like an independent integrative nervous system
(minibrain) inside the walls of the gut. Level 2 consists of the prevertebral
ganglia of the sympathetic nervous system. Levels 3, 4, and 5 are within
the CNS. Sympathetic and parasympathetic signals to the digestive tract
originate at levels 3 and 4 (central sympathetic and parasympathetic
centers) in the medulla oblongata and represent the final common
pathways for the outflow of information from the brain to the gut. Level 5
includes higher brain centers that provide input for integrative functions
at levels 3 and 4.

Autonomic signals to the gut are carried from the brain and spinal cord by
sympathetic and parasympathetic nervous pathways, which represent the
extrinsic component of innervation. Neurons of the ENS form the local
intramural control networks that make up the intrinsic component of the
autonomic innervation. The parasympathetic and sympathetic
subdivisions are identified by the positions of the ganglia that contain the
cell bodies of the postganglionic neurons and by the point of outflow from
the CNS. Comprehensive autonomic innervation of the digestive tract
consists of interactive interconnections between the brain, the spinal cord,
and the ENS.

Pic: A hierarchy of five levels of neural organization determines


the moment-to-moment motor behavior of the digestive tract.
Parasympathetic neurons innervate the gut from the medulla
oblongata and sacral spinal cord.
The cell bodies of parasympathetic neurons projecting to the gut are in
both the brainstem and the sacral region of the spinal cord. The nerve
fibers projecting from these regions of the CNS are motor efferents.

Neuronal cell bodies for motor efferents in the parasympathetic cranial


division reside in the medulla oblongata and transmit information to the
gut via vagus nerves. Motor neuronal cell bodies of the sacral division are
located in the sacral region of the spinal cord and transmit information via
pelvic nerves to the large intestine. Efferent fibers in the pelvic nerves
make synaptic contact with neurons in ganglia located on the serosal
surface of the colon and in ganglia of the ENS deeper within the wall of
the large intestine. Efferent vagal fibers make synaptic connections with
neurons of the ENS in the esophagus, stomach, small intestine, and colon
as well as the gallbladder and pancreas. Efferent vagal nerves transmit
signals to the ENS innervations of the GI musculature to control digestive
processes both in anticipation of food intake and following a meal. This
involves the stimulation and inhibition of contractile behavior in the
stomach, which results from activation of the ENS circuits that control
excitatory or inhibitory musculomotor neurons, respectively.
Parasympathetic efferents to the small and large intestinal musculature
are predominantly stimulatory due to their input to the ENS microcircuits
that control the activity of excitatory musculomotor neurons.

The digestive tract is innervated


by the parasympathetic division
of the autonomic nervous
system. Signals from
parasympathetic centers in the
central nervous system are
transmitted to the enteric nervous
system by the vagus and pelvic
nerves. These signals result in either
contraction (+) or relaxation () of
the digestive musculature.

Sympathetic nerves innervate blood vessels, mucosa, and


muscularis of the gut and suppress gut activity when stimulated.
Sympathetic innervations to the gut exit from the thoracic and lumbar
regions of the spinal cord .Efferent sympathetic fibers leave the spinal
cord in the ventral roots to make their first synaptic connections with
neurons in prevertebral sympathetic ganglia located in the abdomen.
The prevertebral ganglia are the celiac, superior mesenteric, and
inferior mesenteric ganglia. Cell bodies in the prevertebral ganglia
project to the digestive tract, where they synapse with neurons of the ENS
in addition to innervating the bloodvessels, mucosa, and specialized
regions of the musculature.
The sympathetic neurons leaving the spinal cord are called
preganglionic sympathetic neurons; the neurons leaving prevertebral
ganglia to the gut are postganglionic sympathetic neurons.
CNS activation of sympathetic input to the GI tract shunts blood from the
splanchnic to the systemic circulation during exercise and stressful
environmental change. Sympathetic suppression of digestive functions,
including motility and secretion, occurs as a coincident adaptation for
reduced

The digestive tract is innervated by the sympathetic division of


the autonomic nervous system. Preganglionic neurons of the
sympathetic division of the autonomic nervous system project to the gut
from thoracic and upper lumbar segments of the spinal cord. Efferent
sympathetic fibers leave the spinal cord in the ventral roots to make their
first connections with neurons in the prevertebral ganglia in the abdomen.
Cell bodies in the prevertebral ganglia are postganglionic neurons, which
project to the digestive tract where they synapse with neurons of the
enteric nervous system in addition to innervating the blood vessels,
mucosa, and specialized regions of the musculature.

Water Absorption
In human adults, the average daily intake of water is about 2 L. secretions
from the salivary glands, pancreas, liver, and GI tract make up most of the
fluid entering the GI tract (about 7 L). Despite this large volume of fluid,
only 100 mL is lost in the feces. Therefore, the GI tract is extremely

efficient in absorbing water. Water absorption by the GI tract is passive.


The rate of absorption depends on both the region of the intestinal tract
and the luminal osmolality. The duodenum, jejunum, and ileum absorb the
bulk of the water that enters the GI tract daily. The colon normally absorbs
about 1.4 L of water and excretes about 100 mL. It is capable of absorbing
considerably more water (about 4.5 L), however, and watery diarrhea
occurs only if this capacity is exceeded.
Water is absorbed in the gut by osmosis.
Because water absorption is determined by the osmolality difference of
the lumen and the blood, water can move both ways in the intestinal tract
(i.e., secretion and absorption). The osmolality of blood is about 300
mOsm/kg H2O. The ingestion of a hypertonic meal (e.g., 600 mOsm/kg
H2O) initially leads to net water movement from blood to lumen; however,
as the small intestine absorbs the various nutrients and electrolytes, the
luminal osmolality falls, resulting in the net water movement from lumen
to blood. The water of a hypertonic meal is therefore absorbed mainly in
the ileum and colon. In contrast, if a hypotonic meal is ingested (e.g., 200
mOsm/kgH2O), net water movement is immediately from the lumen to the
blood, resulting in the absorption of most of the water in the duodenum
and jejunum.
Electrolyte Absorption
Sodium
The GI system is well equipped to handle the large amount of Na+
entering the GI lumen dailyon average, about 25 to 35 g of Na+ every
day. Around 5 to 8 g is derived from the diet and the rest from salivary,
gastric, biliary, pancreatic, and small intestinal secretions. The GI tract is
extremely efficient in conserving Na+: Only 0.5% of intestinal Na+ is lost
in the feces. The jejunum absorbs more than half of the total Na+, and the
ileum and colon absorb the remainder. The small intestine absorbs the
bulk of the Na+ presented to it, but the colon is most efficient in
conserving Na+.

Several different mechanisms operating at varying degrees in different


parts of the GI tract absorb sodium.
When a meal that is hypotonic to plasma is ingested, considerable
absorption of water from the lumen to the blood takes place,
predominantly through tight junctions and intercellular spaces between
the enterocytes, resulting in the absorption of small solutes such as Na+
and Cl ions. This mode of absorption, called solvent drag, is
responsible for a significant amount of the Na+ absorption by the
duodenum and jejunum, but it probably plays a minor role in Na+
absorption by the ileum and colon because more distal regions of the
intestine are lined by a tight epithelium.
In the jejunum, a Na+/K+-ATPase actively pumps Na+ out of the
basolateral surface of enterocytes ,The result is low intracellular Na+
concentration, and the luminal Na+ enters enterocytes down the
electrochemical gradient, providing energy for the extrusion of H+ into
the lumen (via a Na+/H+ exchanger). The H+ then reacts with HCO3 in
bile and pancreatic secretions in the intestinal lumen to form H2CO3.
Carbonic acid dissociates to form CO2 and H2O. The CO2 readily diffuses
across the small intestine into the blood. Another mode of Na+ uptake is
via a carrier located in the enterocyte brush border membrane, which
transports Na+ together with a monosaccharide (e.g., glucose) or an
amino acid molecule (symport type of transport).
In the ileum, the presence of an Na+/K+-ATPase at the basolateral
membrane also creates a low intracellular Na+ concentration, and luminal
Na+ enters enterocytes down the electrochemical gradient. Sodium
absorption by Na+- coupled symporters is not as great as in the jejunum
because the small intestine has already absorbed most of the
monosaccharides and amino acids. Sodium chloride is transported via two
exchangers located at the brush border membrane. One is a Cl/HCO3
exchanger, and the other is an Na+/H+ exchanger. The downhill
movement of Na+ into the cell provides the energy required for the uphill
movement of the H+ from the cell to the lumen. Similarly, the downhill
movement of HCO3 out of the cell provides the energy for the uphill

entry of Cl into the enterocytes. The Cl then leaves the cell through
facilitated transport. This mode of Na+ uptake is called Na+/H+
Cl/HCO3 counter transport.
In the colon, the mechanisms for Na+ absorption are mostly similar to
those described for the ileum. There is no sugar-coupled or amino acidcoupled Na+ transport because most sugars and amino acids have
already been absorbed.
Sodium is also absorbed here via Na+-selective ion channels in the apical
cell membrane (electrogenic Na+ absorption).
Potassium
The average daily intake of K+ is about 4 g. Absorption takes place
throughout the intestine by passive diffusion through the tight junctions
and lateral intercellular spaces of the enterocytes. The driving force for K+
absorption is the difference between luminal and blood K+ concentration.
The absorption of water results in an increase in luminal K+ concentration,
resulting in K+ absorption by the intestine. In the colon, K+ can be
absorbed or secreted depending on the luminal K+ concentration. With
diarrhea, considerable K+ can be lost. Prolonged diarrhea can be lifethreatening, because the dramatic fall in extracellular K+ concentration
can cause complications such as cardiac arrhythmias.
Chloride
Most of the Cl ions added to the GI tract from the diet and from the
various secretions of the GI system are absorbed.
Intestinal chloride absorption involves both passive and active
processes. In the jejunum, active Na+ absorption generates a potential
difference across the small intestinal mucosa, with the serosal side more
positive than the lumen.
Chloride ions follow this potential difference and enter the bloodstream via
the tight junctions and lateral intercellular spaces. In the ileum and colon,
enterocytes actively take up Cl via Cl/HCO3 exchange, as discussed
above. The presence of other halides inhibits this absorption of Cl.

Bicarbonate
Bicarbonate ions are absorbed in the jejunum together with Na+. The
absorption of HCO3 by the jejunum stimulates the absorption of
Na+ and H2O
Through an Na+/H+ exchanger, H+ is secreted into the intestinal lumen,
where H+ and HCO3 react to form H2CO3, which then dissociates to
form CO2 and H2O. The CO2 diff uses into the enterocytes, where it reacts
with H2O to form H2CO3 (catalyzed by carbonic anhydrase). H2CO3
dissociates into
HCO3 and H+, and the HCO3 then diffuses into the blood.
In the ileum and colon, HCO3 is actively secreted into the lumen in
exchange for Cl. This secretion of HCO3 is important in buffering the
decrease in pH resulting from the short-chain fatty acids produced by
bacteria in the distal ileum and colon.

Calcium
The amount of Ca2+ entering the GI tract is about 1 g/day, approximately
half of which is derived from the diet. Most dietary Ca2+ is derived from
meat and dairy products. Of the Ca2+ presented to the GI tract, about
40% is absorbed. Several factors affect Ca2+ absorption. For instance, the
presence of fatty acid can retard Ca2+ absorption by the formation of
Ca2+ soap. In contrast, bile salt molecules form complexes with Ca2+
ions, which facilitate Ca2+ absorption.
Calcium absorption takes place predominantly in the duodenum and
jejunum, is mainly active, and involves three steps:
(1) Enterocytes take up calcium by passive diffusion through a Ca2+
channel, because there is a large Ca2+ concentration gradient; the
luminal Ca2+ is about 5 to 10 mM,whereas free intracellular Ca2+ is
about 100 nM.
(2) Once inside the cell, Ca2+ is complexed with Ca2+-binding protein,

calbindin D (CaBP).
(3) At the basolateral membrane, Ca2+ is extruded from the enterocytes
via the Ca2+-ATPase pump. Calcium uptake by enterocytes, the level of
CaBP in the cells, and transport by Ca2+-ATPase pumps are increased by
1,25-dihydroxyvitamin D3. Once inside the cell, the Ca2+ ions are
sequestered in the ER and Golgi membranes by binding to the CaBP in
these organelles.
Calcium absorption by the small intestine is regulated by the circulating
plasma Ca2+ concentration. Lowering of the Ca2+ concentration
stimulates the release of parathyroid hormone, which stimulates the
conversion of vitamin D to its active metabolite, 1,25-dihydroxyvitamin
D3, in the kidney.
This, in turn, stimulates the synthesis of CaBP and the Ca2+-ATPase by
the enterocytes (Fig. 26.26). Because protein synthesis is involved in the
stimulation of Ca2+ uptake by parathyroid hormone, a lapse of a few
hours usually occurs between the release of parathyroid hormone and the
increase in Ca2+ absorption by the enterocytes.

Magnesium
Humans ingest about 0.4 to 0.5 g/d of Mg2+. The absorption of Mg2+
seems to take place along the entire small intestine, and the mechanism
involved seems to be passive.
Vitamin Absorption
An organic compound is called a vitamin because it cannot be synthesized
by the body and must be obtained from diet
For absorption, vitamins are classified in two ways:
1. Water soluble
2. Fat-soluble
13 vitamins are universally recognized
9 water soluble and 4 fat soluble

The 9 water soluble are the 8 B Vitamins and C Vitamin


The 4 Fat Soluble are A, D,E and K
Note that water-soluble vitamins are easily dissolved in water and are also
readily been excreted from the body.
The urinary output is a strong predictor of B-Vitamin and C Vitamin
consumption.
Vitamins have many diverse cell functions and many are essential for
metabolic reactions.
Vitamins act as both catalysts and substrates in chemical reactions
of the body. When acting as a catalyst, vitamins are bound to enzymes
and are called cofactors (e.g., vitamin K forms part of the proteases
involved in blood clotting).
Vitamins can also act as coenzymes to carry chemical groups
between enzymes (e.g., folic acid carries a carbon group methylene in the
cell).
Fruits and vegetables are good sources of vitamins.
Fat-soluble vitamins: A, D, E, and K
The principal form of vitamin A is retinol; the aldehyde(retinal) and the
acid (retinoic acid) are also active forms of vitamin A. Retinol can be
derived directly from animal sources or through conversion from bcarotene (found abundantly in carrots) in the small intestine.
Micellar solubilization renders vitamin A water-soluble, and the small
intestine absorbs it passively. The unesterified retinol is then complexed
with retinol-binding protein type 2, and the complex serves as a substrate
for the re-esterifi cation of the retinol by the enzyme lecithin:retinol
acyltransferase. The retinyl ester is incorporated in chylomicrons and
taken up by the liver.
Vitamin A is stored in the liver and released to the circulation bound to
retinol-binding protein only when needed.

Vitamin A is important in the production and regeneration of rhodopsin of


the retina and in the normal growth of the skin. People with vitamin A
deficiency develop night blindness and skin lesions.
Vitamin D is a group of fat-soluble compounds collectively
known as the calciferols. Vitamin D3 (also called cholecalciferol or
activated dehydrocholesterol) in the human body is derived from two
main sources: the skin, which contains a rich source of 7dehydrocholesterol, which is rapidly converted to cholecalciferol when
exposed to ultraviolet light, and dietary vitamin D3. Like vitamin A,
vitamin D3 is absorbed by the small intestine passively and is
incorporated into chylomicrons. During the metabolism of chylomicrons,
vitamin D3 is transferred to a binding protein in plasma called the
vitamin Dbinding protein.
Unlike vitamin A, vitamin D is not stored in the liver but is distributed
among the various organs depending on their lipid content. In the liver,
vitamin D3 is converted to 25-hydroxycholecalciferol,which is
subsequently converted to the active hormone 1,25dihydroxycholecalciferol in the kidneys. The latter enhances Ca2+ and
phosphate absorption by the small intestine and mobilizes Ca2+ and
phosphate from bones.
Vitamin D is essential for normal development and growth and the
formation of bones and teeth. Vitamin D deficiency can result in rickets, a
disorder of normal bone ossification manifested by distorted bone
movements during muscular action.
The major dietary vitamin E is a-tocopherol. Vegetable oils are rich in
vitamin E. It is absorbed by the small intestine by passive diffusion and
incorporated into chylomicrons.
Unlike vitamins A and D, vitamin E is transported in the circulation
associated with lipoproteins and erythrocytes.
Vitamin E is a potent antioxidant and therefore prevents lipid peroxidation.
Tocopherol defi ciency is associated with increased red cell susceptibility

to lipid peroxidation, which may explain why the red cells are more fragile
in people with vitamin E defi ciency than in healthy people.
Vitamin K can be derived from green vegetables in the diet or the gut
flora. The vitamin K derived from green vegetables is in the form of
phylloquinones. Vitamin K derived from bacteria in the small intestine is
in menaquinones.
The small intestine takes up phylloquinones via an energy-dependent
process from the proximal small intestine.
In contrast, menaquinones are absorbed from the small intestine
passively, depending only on the micellar solubilization of these
compounds by bile salts. Vitamin K is incorporated into chylomicrons. It is
rapidly taken up by the liver and secreted together with VLDLs. No carrier
protein for vitamin K has been identified.
Vitamin K is essential for the synthesis of various clotting factors by the
liver. Vitamin K deficiency is associated with bleeding disorders.

Water-soluble vitamins: C, B1, B2, B6, B12,


niacin, biotin, and folic acid
Most of the water-soluble vitamins are absorbed by the small intestine by
both passive and active processes.
The major source of vitamin C (ascorbic acid) is green vegetables and
fruits. It plays an important role in many oxidative processes by acting as
a coenzyme or cofactor. It is absorbed mainly by active transport through
the transporters in the ileum. The uptake process is sodium-dependent.
Vitamin
C deficiency is associated with scurvy, a disorder characterized by
weakness, fatigue, anemia, and bleeding gums.

Vitamin B1 (thiamine) plays an important role in carbohydrate


metabolism. The jejunum absorbs thiamine passively as well as by an
active, carrier-mediated process.
Thiamine deficiency results in beriberi, characterized by anorexia and
disorders of the nervous system and heart.
Vitamin B2 (riboflavin) is a component of the two groups of
flavoproteinsflavin adenine dinucleotide and flavin mononucleotide.
Riboflavin plays an important role in metabolism. It is absorbed by a
specific, saturable, active transport system located in the proximal small
intestine.
Its deficiency is associated with anorexia, impaired growth, impaired use
of food, and nervous disorders.
Niacin plays an important role as a component of the coenzymes NAD(H)
and NADP(H), which participate in a wide variety of oxidationreduction
reactions involving H+ transfer.
At low concentrations, the small intestine absorbs niacin by Na+dependent, carrier-mediated facilitated transport. At high concentrations,
it is absorbed by passive diffusion. Niacin has been used to treat
hypercholesterolemia, for the prevention of coronary artery disease. It
decreases plasma total cholesterol and LDL cholesterol, yet increases
plasma HDL cholesterol.
Niacin deficiency is characterized by many clinical symptoms including
anorexia, indigestion, muscle weakness, and skin eruptions. Severe
deficiency leads to pellagra, a disease characterized by dermatitis,
dementia, and diarrhea.
Vitamin B6 (pyridoxine) is involved in amino acid and carbohydrate
metabolism. Vitamin B6 is absorbed throughout the small intestine by
simple diffusion. A deficiency of this vitamin is oft en associated with
anemia and central nervous system disorders.
Biotin acts as a coenzyme for carboxylase, transcarboxylase, and
decarboxylase enzymes, which play an important role in the metabolism
of lipids, glucose, and amino acids. At low luminal concentrations, biotin is

absorbed by the small intestine by Na+-dependent active transport. At


high concentrations, biotin is absorbed by simple diff usion. Biotin is so
common in food that deficiency is rarely observed. However,
biotin deficiency occurs frequently when parenteral nutrition(nutrition
administered intravenously) is administered for a long period.
Folic acid is usually found in the diet as polyglutamyl conjugates
(pteroylpolyglutamates). It is required for the formation of nucleic acids,
the maturation of red blood cells, and growth. An enzyme on the brush
border degrades pteroylpolyglutamates to yield a monoglutamylfolate,
which is taken up by enterocytes by facilitated transport. Inside
enterocytes, the monoglutamylfolate is released directly into the
bloodstream or converted to 5-methyltetrahydrofolate before exiting the
cell. A folate-binding protein binds the free and methylated forms of folic
acid in plasma. Folic acid deficiency causes a fall in plasma and red cell
folic acid content and, in its most severe form, the development of
megaloblastic anemia, dermatologic lesions, and poor growth.
The discovery of vitamin B12 (cobalamin) followed from the
observation that patients with pernicious anemia who ate large
quantities of raw liver recovered from the disease. Subsequent analysis of
liver components isolated the cobalt-containing vitamin, which plays an
important role in the production of red blood cells. A glycoprotein secreted
by the parietal cells in the stomach called the intrinsic factor binds
strongly with vitamin B12 to form a complex that is then absorbed in the
terminal ileum through a receptor-mediated process
Vitamin B12 is transported in the portal blood bound to the protein
transcobalamin. People who lack the intrinsic factor fail to absorb
vitamin B12 and develop pernicious anemia.

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