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Mittal RK. Motor Function of the Pharynx, Esophagus, and its Sphincters. San Rafael (CA): Morgan & Claypool Life Sciences; 2011.

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Motor Function of the Pharynx, Esophagus, and its Sphincters.

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Peripheral Mechanisms of Peristalsis

Several observations support that the mechanisms of peristalsis resides in the esophageal wall. Pattern of neural innervation and activation in the myenteric plexus are important determinants of peristalsis. Furthermore, pattern of spread of contraction in the muscles (myogenic) may play an important role in esophageal peristalsis. First, electrical stimulation of the peripheral end of cervical vagus nerve, which undoubtedly stimulates all vagal efferent fibers simultaneously and eliminates the possibility of sequential activation of vagal efferent fibers, can elicit peristaltic contraction depending upon the electrical stimulus parameters [136] (Figure 17A). Second, smooth muscle esophagus removed from the animal and placed in an organ bath (devoid of extrinsic innervations) demonstrates secondary peristalsis, with ascending contractions and descending relaxation [137]. Third, circular muscle strips studied in an organ bath show an increasing latency gradient from the cranial to caudal direction [138,139] (Figure 17B). In other words, when muscles from different levels in the esophagus are stimulated at the same time, they contract following a certain time period after the cessation of electrical stimulus, the so-called latency period. Muscle strips, devoid of extrinsic innervations, from the distal esophagus have longer latency period as compared to the proximal esophagus. Mechanical pinching and distension of the esophagus in vitro also evoke peristalsis in the smooth muscle esophagus, suggesting that the mechanism of peristalsis resides in the periphery, i.e., in the esophageal wall [140,141].

FIGURE 17. Mechanism of peristalsis in the smooth muscle esophagus.


Mechanism of peristalsis in the smooth muscle esophagus. (A) Peristalsis elicited by electrical stimulation of the peripheral end of cervical vagus nerve in the opossum smooth muscle esophagus—note that even though all efferent fibers were stimulated (more...)

During the actual period of stimulation (electrical—vagus nerve/intramural or mechanical—balloon distension) or the latency period, intracellular recordings of the smooth muscles show hyperpolarization (decrease in the resting membrane potential) followed by depolarization and spike bursts [142,143]. Hyperpolarization is equivalent of inhibition or muscle relaxation and depolarization with spike bursts of muscle contraction. A swallow activates an immediate hyperpolarization along the length of esophagus that induces muscle relaxation, the duration of which corresponds to the latency of contraction, followed by depolarization and spike burst (contraction) [143]. The latency period as well as hyperpolarization is induced by activation of inhibitory nerves through the release of nitric oxide [144]. On the other hand, it is not totally clear if depolarization and spike discharges are due to passive rebound phenomenon from hyperpolarization or release of an excitatory neurotransmitter (acetylcholine). It is suggested that nerve-induced depolarization, following hyperpolarization, depends upon the production of eicosanoids. This has been shown in the longitudinal muscles of esophagus [145] and colonic taenia coli [146]. With an increase in the frequency of electrical stimulus, the latency period decreases in the proximal esophagus but increases in the distal esophagus. Furthermore, latency period in the proximal esophagus is more susceptible to atropine (anticholinergic) than the distal esophagus [147]. Based on the above observation, gradients of cholinergic and nitrergic innervations are suggested along the length of the esophagus, with the former being greater in the proximal and the latter more in the distal esophagus [147]. Even though above observation would be consistent with the anatomical evidence of gradients in the density of myenteric plexus along the esophageal length, numbers of acetylcholinestrase positive neurons do not differ along the length of esophagus [148]. Furthermore, there are no anatomical data for the differences in the nitrergic neurons along the length of the esophagus. Organ bath studies of the isolated esophagus suggest that descending hyperpolarization is mediated through a long descending neuron, at least more than 3 cm in size, and there are no synapses in this pathway [137].

Intrinsic differences in smooth muscle responses along the esophagus may also be the result of quantum or effects of released neurotransmitter on the muscles from different regions. Resting membrane potential along the esophagus is less negative distally, which may be related to the gradient of potassium content along the smooth muscle esophagus [149,150]. A number of regional myogenic differences along the length of the esophagus also exist [151154]: (1) a more depolarized resting membrane potential due to sodium permeability and increase in the density of voltage-dependent potassium channels proximally [155]; (2) regional differences in the soluble N-ethylenemaleimide sensitive factors attachment protein receptor (SNARE) protein SNAP-25 [153], which regulate potassium channels [151]; (3) response to stretch and cholinergic stimulation, with strips from more proximal regions being more responsive [152]; (4) increased expression and current density of L-type calcium channels in the proximal versus the distal smooth muscle esophagus [153].

Studies in the humans highlight the significance of balance in the excitatory and inhibitory innervation in the genesis of spastic motor disorders [156159]. Nitric oxide antagonist decreases latency of contraction in the distal esophagus and converts peristaltic contraction into a simultaneous one. Atropine delays the latency of contraction in the proximal esophagus to increase the velocity of peristalsis [160]. These observations support the concept that in patients with spastic motor disorders of the esophagus, there is an imbalance between the inhibitory and excitatory nerve activity.

There is also evidence to suggest myogenic mechanism of peristalsis [161163]. Peristalsis can be recorded in live animals following administration of tetrodotoxin (TTX), which blocks all sodium channels' mediated action potential in the all neurons and its processes. Myogenic contractions and peristalsis can be elicited by the long pulse duration electrical current that activates muscle directly, by esophageal distention, by muscle membrane depolarization using high concentrations of K+, and pharmacologic stimulation. It is suggested that the muscle-to-muscle communication such that depolarization of one smooth muscle cell will result in electrotonic spread of current to adjacent muscle cells in an aboral direction [164].

Copyright © 2011 by Morgan & Claypool Life Sciences.
Bookshelf ID: NBK54270
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