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An Examination
of factors that Affect the Lower Esophageal Sphincter  During Digestion

Human Physiology

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BIOM 525- D01

Kimberly Mitchell

December 3,2017


The lower esophageal sphincter plays a
vital role in ensuring the bolus remains in the stomach. Various factors
influence the normal functioning of the lower esophageal sphincter. Factors
include: release of neurotransmitters, pressure, and relaxation or contraction
of smooth muscles.  

The lower esophageal sphincter (LES) has
multiple functions. (5)  LES regulates esophageal
emptying and allows the forward movement of the bolus. It prevents air from
moving back into the pharynx when opened. It also protects against retrograde regurgitation
of gastric contents from moving into the proximal esophagus and the pharynx. LES
is composed of circular smooth muscles. The two circular muscles in the LES are
the gastric clasps and the gastric sling muscles. (4) These muscles form a
pressure barrier in the proximal part of the stomach. The gastric sling muscle
is a part of the high-pressure zone on the greater curvature side of the
gastric cardia. The gastric clasp muscle is a part of the high-pressure zone of
the lesser curvature side of the gastric cardia. The circular muscles, along
with the longitudinal muscles and upper esophageal sphincter (UES) work
together to form the high-pressure zone. These muscles serve as a antireflux
barrier in the esophagus. LES basal tone also contributes to the increase in
pressure at the esophageal gastric junction. When the high-pressure zone is being
partially relaxed, there is an increase in intra-abdominal pressure. This is a result
from the response of deglutition and contraction in the esophagus.

The LES basal tone is responsible for
regulation of the bolus movement from the esophagus to the stomach. (6) Basal
tone is myogenic and primarily originates in the smooth muscle of the
esophagus. LES’s smooth muscles are more depolarized than muscles in the body.

The more negative membrane leads to the activation of calcium channels. The
influx of calcium leads to the maintenance of LES tone.

LES is asymmetric and is sensitive to cholinergic
stimulation. (4) The higher sensitivity is due to the binding of muscarinic
receptors as well as some neurotransmitters: dopamine, phenylephrine, and
isoprenaline. The opposite occurs with inhibition of acetylcholine. Atropine is
an anticholinergic drug. Atropine decreases LES tone, significantly more on the
left side of the sphincter. It blocks acetylcholine from assisting with muscle

The circular muscle contraction and the longitudinal
muscle contraction assist with the peristalsis movement by moving contents away
from the mouth and out of the oral cavity.  (5) Peristalsis is due to the contraction of
the proximal portion of the esophagus and the relaxation of the distal portion
of the esophagus.  During peristalsis,
the lumen is distending which can induce LES relaxation. The greater the
distension in the esophagus, the greater the LES relaxation. The synchronous
relaxation of the circular and longitudinal muscles is a result of neuronal
damage.  The simultaneous relaxation
stimulates the inhibitory efferent. The inhibitory efferent sends a signal to
release nitric oxide. Nitric oxide is an inhibitory neurotransmitter in the
esophagus. The blockage of the vagal efferent abolishes peristalsis in the
esophagus. This is due to nitric oxide creating a more hyperpolarized membrane,
reducing the esophagus’s ability to generate action potential. This inhibition
leads to transient lower esophageal sphincter relaxation.

Transient lower esophageal sphincter relaxation
(TLESR) is a motor pattern that is designed to transport contents back through
the esophagus. (5)  TLESR usually last approximatively
10-30 seconds. During this time, it increases the gastro-esophageal reflux. Examples
of retrograding in the esophagus are belching and vomiting. In addition to
TLESR, there is an inhibition of the crural diaphragm longitudinal muscle
contraction. Because of TLESR, the esophagus is inhibited during deglutition. During
TLESR, there is a selective contraction in the longitudinal muscle of the distal
portion of the esophagus. The selective longitudinal contraction that is taking
place creates a movement that is the reverse of peristalsis. Longitudinal
muscles remain contracted throughout the entire length of TLESR but circular
muscles remain relaxed. In normal peristalsis, there is a greater axial
shortening of the circular muscle compared to the longitudinal muscle layer.

But during TLESR, the reverse is happening; there is a greater shortening of the
longitudinal muscle compared to the circular muscle layer. At the end of TLESR,
there is an abrupt shift in contraction resulting in a normal peristalsis
pattern. The sudden change is a result from the synchrony of contraction in the
circular and muscular layer. Also, a stimulus in the pharynx can induce normal
primary peristalsis. The stimulus induces the axial shortening of the circular muscle
layer in the distal portion of the esophagus allowing the longitudinal muscle
layer to contract in the proximal portion of the esophagus. This mechanism allows
for the LES to transport the bolus into the stomach.

After LES relaxation, contractions
reoccur. (6) Basal tone is then restored in the esophagus. This change is due
to deglutition or end of TLESR. Contractions and peristalsis reoccur in the esophageal
body. Sensory input triggers the motor activity in the muscles of the
esophagus. Excitatory nerves are released allowing LES contraction. Muscarinic
receptors are located on the smooth muscles. The acetylcholine muscarinic receptors
release calcium from the endoplasmic reticulum and activate calmodulin. Calcium
binds to calmodulin to induce contraction on the smooth muscles. Even though
peristalsis is involuntary, contractions assist with the triggering the
wave-like movement in the esophagus.

Peristalsis moves gastric materials from
a higher pressure to a lower pressure. LES has a greater pressure than the
stomach. (4) The time it takes for the bolus to reach the stomach is dependent
upon gravity. Once the bolus reaches the LES, it will pass through the
sphincter. After entering into the stomach, the sphincter will contract to
prevent retrograde reflux.

The stomach is responsible for storing,
mixing, and emptying gastric contents. (1)  The proximal part of the stomach serves as a
reservoir. The distal portion of the stomach is responsible for mixing and
emptying gastric contents. The motion of peristalsis allows gastric mixing and anterograde
flow.   During peristalsis contraction, the lumen
becomes narrower as the contents approach the gastric pylorus. Before the
gastric contents approaches the pylorus, it passing the antrum. The antrum has
an extremely high velocity. Retropulsion is occurring in the antrum due to the narrowed
lumen by the peristalsis contractions. Recirculation is taking place in between
contraction. There is a large recirculation occurring in the antrum and the
distal portion of the stomach.

The changing in one’s posture and amount
of ingested volume that is entered into the stomach affects gastric mixing. (1)
The recirculation in the antrum is dependent upon posture. Recirculation can
occur in two places in the stomach, inside and outside of the antrum. Normal
recirculation occurs inside the antrum.  When
one’s posture is changed from the upright position, it creates minor and major
changes in the mixing of gastric contents and flow. In the prone position, there
is the largest amount of recirculation occurring. It also allows for a large
volume of gastric contents. The greater the volume in the antrum cause gastric mixing
outside of the normal recirculation area. The contents inside the antral recirculation
is well mixed as compared to the contents that is being outside. The poor
mixing is due to the recirculation occurring in the outer regions. This
mechanism is taking place in the proximal region of the stomach. Also, in the
supine and left position, gastric contents are being mixed outside the antral
recirculation region. In these positions, prone, supine, and left position
there is an increase in total volume content in the proximal part of the
stomach.  The increase volume near the
proximal part of the stomach creates lower pressure around the LES. The abnormal
lower pressure in the LES prevents the antireflux barrier. (2) This creates a
relaxed LES and a delayed recovery of gastric tone. The relaxed LES and reflux
delays the onset of the stomach emptying gastric contents. (2)  LES relaxation allows gastric contents and
gastric acids to enter into the esophagus. (2) The esophagus is hypersensitive.

(3) The chemical stimulation from the acid exposure ignites inflammatory
mediators. (3) It can trigger heartburn, acid reflux events, and cancer
overtime. (3)

It is essential to have an efficient
lower esophageal sphincter. The sphincter plays various roles in the digestion
of food. The most essential role is to prevent the bolus from re-entering the
esophagus after it has been transported to the stomach. If normal functioning
of the sphincter is compromised gastric contents will re-enter into the esophagus.

This creates various disorders in individuals once triggered. The most commonly
disorder affiliated with gastric reflux is gastroesphageal reflux disease (GERD).