How does swallowing occur with peristalsis

From the above discussion it is clear that both NO and acetylcholine are crucial neurotransmitters in generation of the peristaltic wave. Nitric oxide produces hyperpolarization of the circular smooth muscle cell membrane via a cyclic guanosine monophosphate cGMP -dependent pathway, 89, 90 thereby causing inhibition of voltage-dependent calcium entry. There has been considerable controversy surrounding the mechanisms whereby NO induces membrane hyperpolarization.

In further support of this, NO donors were reported to activate multiple types of potassium channels and whole cell potassium currents in different smooth muscles, including esophageal. However, selective potassium channel blockers failed to abolish the nitrergic IJP in opossum esophageal circular smooth muscle, 93, 94 suggesting that opening of potassium channels may not underlie the hyperpolarization caused by neurally released NO.

Based on experiments utilizing chloride substitution and application of the anion channel blocker 4,4'—diisothiocyanostilbine—2,2'—disulfonic acid, Crist et al. Subsequently, Zhang et al. More recently, Zhang and Paterson reported that the nitrergic IJP could be blocked by two different calcium-activated chloride channel blockers, namely niflumic acid and 9-anthroic acid. Furthermore, they provided evidence that the nitrergic IJP is dependent on activation of myosin light chain kinase.

At rest, the membrane potential of esophageal circular smooth muscle cells shows apparently random membrane potential fluctuations of 1 to 3 mV. Inhibitors of sarcoplasmic reticulum function or blockers of chloride channels markedly attenuate these random fluctuations, suggesting that they are due to spontaneous activation of chloride channels, primed by calcium release from the sarcoplasmic reticulum.

Acetylcholine affects many ionic currents in esophageal circular smooth muscle including calcium-sensitive chloride and nonselective cation currents. Chloride currents cause depolarization of the smooth muscle membrane, which in turn leads to entry of extracellular calcium via voltage-sensitive calcium channels.

Activation of nonselective cation channels does not lead to significant membrane depolarization. Their activation may result in calcium entry by non—voltage-dependent mechanisms.

The second messenger pathways involved in acetylcholine-induced contraction are complex, and have recently been reviewed Figure 8.

Acetylcholine acts on muscarinic type 2 M 2 receptors that are linked to G i3 -type G proteins within the muscle membrane. Of interest, esophageal peristalsis can be induced in the smooth muscle esophagus in the presence of tetrodotoxin, which blocks all sodium channel—mediated action potentials in neurons.

It is believed that there is polarization of 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. Secondary peristalsis refers to peristalsis activated by esophageal distention.

This can occur physiologically by food left behind after the primary peristaltic wave has passed, or by refluxed contents from the stomach.

Unlike primary peristalsis, secondary peristalsis is not accompanied by deglutition with associated pharyngeal and upper esophageal sphincter motor function. In the striated muscle esophagus, distention activates a peristaltic reflex that is mediated by central mechanisms; distention activates vagal afferents, which in turn leads to sequential vagal efferent discharge to the striated musculature of the proximal esophagus.

Indeed, luminal distention of an esophagus excised and placed in a tissue bath results in a peristaltic contraction. A similar, atropine-sensitive contraction orad to the balloon is also seen in humans. During the distending stimulus there is a descending inhibitory discharge, mediated predominantly by NO , which results in hyperpolarization and inhibition of the circular smooth muscle.

This peristaltic reflex is quite different from that described in the intestine, where the proximal excitation does not involve extrinsic innervation. Rather, descending nitrergic neurons appear to be activated directly by the distending stimulus and send long descending inhibitory neural connections to the distal esophagus.

Understandably, investigators have focused on the role of the circular smooth muscle in esophageal peristalsis; however, the longitudinal muscle also contracts in sequential fashion during peristalsis and appears to play a role in bolus transport.

To date, studies on the physiology of the longitudinal muscle have focused entirely on the smooth muscle esophagus. Whereas it is easy to conceptualize how aborally progressive lumen occluding contractions of the circular muscle serve to push the bolus toward the stomach, it is less obvious how longitudinal muscle contraction might be involved in this process.

It has been proposed that the longitudinal smooth muscle contraction may facilitate peristalsis by two mechanisms: 1 by shortening the esophagus, the esophageal radius must increase, thereby increasing the lumen size ahead of the oncoming bolus ; 2 longitudinal contractions tend to slide the esophagus over the bolus and increase the density of the circular muscle fibers orad to the bolus, which in turn increase the efficiency of the circular muscle contraction 2.

Recent studies using a mathematical model based on fluid theory have provided evidence that local longitudinal muscle contraction results in marked reduction in local pressure and shear stress in the zone of circular muscle contraction, thereby reducing the peak contractile pressure required for bolus transit.

Studies in the opossum have shown that the longitudinal muscle contracts sequentially in an aboral direction during primary peristalsis. The duration of longitudinal muscle contraction also appears to vary along the esophagus.

Similar to circular muscle, contraction is longer distally than proximally. In vivo studies in the opossum model have also shown that the primary neurotransmitter involved in longitudinal smooth muscle contraction is acetylcholine. The muscarinic antagonist atropine virtually abolishes longitudinal muscle contraction and esophageal shortening in response to swallowing and vagal stimulation.

In vitro studies have also shown that longitudinal muscle contraction is predominantly mediated by cholinergic neurons; however, with certain stimulus parameters a slowly developing and sustained longitudinal muscle contraction can be evoked, which is abolished by substance P desensitization. However, it may play a role in the reflex longitudinal muscle contraction that occurs with acid reflux into the esophagus.

Nitric oxide has been reported to cause paradoxical contraction of esophageal longitudinal smooth muscle, 86, , but it is unclear whether this neurotransmitter is involved in physiologic contraction of this muscle layer. Nitric oxide synthase inhibition appeared to decrease swallow-induced esophageal shortening in the cat, but evidence for a NO-mediated neural response could not be found in vitro in this species.

Although there is evidence that the longitudinal smooth muscle may participate in deglutitive inhibition, there is no evidence to date that this is related to direct inhibitory innervation to the longitudinal smooth muscle. Elegant studies in which electrical activity was recorded from a flap of isolated longitudinal smooth muscle in vivo showed no evidence of an inhibitory junction potential occurring during primary peristalsis.

Little is known about the physiologic role of the muscularis mucosa during peristalsis. It may contract primarily in response to luminal stimuli, thereby evoking movement of esophageal mucosa. It may also serve to hold the normally loosely attached overlying mucosa in place, thereby preventing excessive movement of the mucosa during bolus movement 2. Studies on the physiology and pharmacology of this muscle layer have been carried out.

There also appears to be a more sustained or tonic contraction due to release of substance P. Esophageal peristalsis, which can be triggered by either swallowing or local esophageal distention, serves to propel esophageal contents into the stomach. This is orchestrated by a complicated interaction between the central nervous system and the myenteric plexus, with the latter predominating in the smooth muscle esophagus. Esophageal peristalsis consists of sequential contraction of the circular muscles of the muscularis propria, which is largely mediated by acetylcholine.

This sequential contraction serves to occlude the esophageal lumen and push the bolus aborally. An important component in this process is the nitrergic inhibition of the circular smooth muscle that occurs aboral to the oncoming bolus.

In addition, sequential contraction of longitudinal muscle also occurs during peristalsis. This serves to shorten the esophagus and increase the cross-sectional diameter, thereby facilitating bolus transport. There remains much to be learned about the physiologic control of esophageal peristalsis, including 1 the precise mechanisms whereby cholinergic and noncholinergic mainly nitrergic innervations interact to generate a peristaltic wave; 2 the cellular mechanisms involved in the nitrergic inhibition of esophageal circular smooth muscle; 3 the role of interstitial cells of Cajal in coordinating esophageal peristalsis; and 4 the role of other neurotransmitters in modulating peristalsis.

Further understanding of the basic physiology underlying esophageal peristalsis will serve as a foundation for improved treatment of patients with dysphagia and chest pain due to esophageal motor dysfunction.

This page has been archived and is no longer updated Jump to main content Jump to navigation nature. Search Advanced search. Top of page Key Points Esophageal peristalsis results from sequential contraction of circular muscle, which serves to push the ingested food bolus toward the stomach. Esophageal longitudinal muscle may also play a role in peristalsis.

Swallow-induced peristalsis is called primary peristalsis, and the peristalsis elicited by esophageal distention is called secondary peristalsis. Peristaltic contractions are always preceded by inhibition that, in the case of primary peristalsis, is called deglutitive inhibition. Peristalsis in the striated muscle part of the esophagus is dependent on central mechanisms, involving sequential activation of vagal lower motor neurons in the vagal nucleus ambiguus.

Peristalsis in the smooth muscle of the esophagus is dependent on both central and peripheral mechanisms. The central mechanism involves patterned activation of the preganglionic neurons in the dorsal motor nucleus of the vagus that project onto inhibitory and excitatory neurons in the esophageal myenteric plexus. The peripheral mechanism involves regional differences in the inhibitory and excitatory intramural nerves and intrinsic properties of the muscle.

Intramural inhibitory nerves act by releasing nitric oxide NO and vasoactive intestinal peptide, whereas the excitatory nerves release acetylcholine and substance P. Top of page Introduction The esophagus is a hollow muscular tube, closed proximally and distally by muscular sphincters. Top of page Methods of Study A number of methodologies have been used to study motility of the esophagus. Figure 1: Primary peristalsis as recorded by an intraluminal manometry catheter. Video 1: Videofluoroscopy of deglutition and primary peristalsis.

View movie file : Video 1: Videofluoroscopy of deglutition and primary peristalsis. Top of page General Description of Peristalsis Figure 1 With deglutition, the peristaltic wave follows immediately after the UES relaxation, producing a lumen-occluding contraction of the esophageal circular muscle. Figure 2: Diagrammatic representation of deglutitive inhibition. Top of page Peristalsis in the Striated Muscle Esophagus Like striated muscle in other parts of the body, the striated muscle segment of the esophagus is dependent on excitatory nerve activity from lower motor neurons.

Top of page Peristalsis in the Smooth Muscle Esophagus Control of peristalsis in the smooth muscle segment of the esophagus is more complicated than in the adjacent striated muscle segment. Peripheral Neurogenic Control The peripheral neuromuscular control mechanisms involved in peristalsis of the esophageal circular smooth muscle has been an area of intense interest and investigation for many years.

Figure 3: Schematic representation of esophageal contractions. Figure 4: Electrical stimulation of intrinsic nerves in circular smooth muscle strips. Figure 5: Simultaneous recording of electrical and mechanical activity in opossum smooth muscle esophagus.

Figure 6: Model showing the marked delay in onset of distal esophageal contractions during peristalsis. Top of page Neurotransmitters Involved in Esophageal Peristalsis: Evidence of Dual Peripheral Innervation Vagal efferent neurons involved in esophageal peristalsis synapse on both inhibitory and excitatory myenteric neurons.

Figure 7: Evidence of dual innervation of esophageal peristalsis. Top of page Ionic and Second Messenger Mechanisms of Esophageal Circular Smooth Muscle Contraction From the above discussion it is clear that both NO and acetylcholine are crucial neurotransmitters in generation of the peristaltic wave. Figure 8: Pathways involved in acetylcholine-induced contraction of esophageal circular smooth muscle.

Top of page Myogenic Mechanisms of Esophageal Peristalsis Of interest, esophageal peristalsis can be induced in the smooth muscle esophagus in the presence of tetrodotoxin, which blocks all sodium channel—mediated action potentials in neurons.

Top of page Secondary Peristalsis Secondary peristalsis refers to peristalsis activated by esophageal distention. Top of page Conclusion Esophageal peristalsis, which can be triggered by either swallowing or local esophageal distention, serves to propel esophageal contents into the stomach. Top of page Ancillary details. Diseases of the Esophagus. New York: Springer-Verlag, Esophageal motility. In: Wood JD, ed. Handbook of Physiology: The Gastrointestinal System. Miller AJ.

Deglutition Physiol Rev ; 62 — Functional anatomy and physiology of swallowing and esophageal motility. The Esophagus , 3rd ed. Esophageal motor function. In: Yamada T, ed. Textbook of Gastroenterology , 3rd ed. Esophageal motor and sensory function and motor disorders of the esophagus.

Philadelphia: WBSaunders, — Multichannel intraluminal impedance in esophageal function testing and gastroesophageal reflux monitoring. J Clin Gastroenterol ; 37 3 — Correlation of high frequency esophageal ultrasonography and manometry in the study of esophageal motility. Gastroenterology ; — A novel ultrasound technique to study the biomechanics of the human esophagus in vivo. Esophageal manometry in 95 healthy adult volunteers. Variability of pressures with age and frequency of "abnormal" contractions.

Dig Dis Sci ; 32 — Effect of dry swallows and wet swallows of different volumes on esophageal peristalsis J Appl Physiol ; 38 — Is the primary peristaltic contraction of the canine esophagus bolus-dependent? Gastroenterology ; 65 — Studies on the necessity of a bolus for the progression of secondary peristalsis in the canine esophagus Gastroenterology ; 67 — ChemPort El Ouazzani T, Mei N. Electrophysiologic properties and role of the vagal thermoreceptors of lower esophagus and stomach of cat Gastroenterology ; 83 — Powerpoint slides on Peristalsis.

Images of Peristalsis. Photos of Peristalsis. Videos on Peristalsis. Cochrane Collaboration on Peristalsis. Bandolier on Peristalsis. TRIP on Peristalsis. Ongoing Trials on Peristalsis at Clinical Trials.

Trial results on Peristalsis. Clinical Trials on Peristalsis at Google. FDA on Peristalsis. CDC on Peristalsis. Books on Peristalsis. Peristalsis in the news. Be alerted to news on Peristalsis. News trends on Peristalsis. Blogs on Peristalsis. Healthcare providers diagnose esophageal cancer in more than 17, people every year.

Risk factors include a severe type of reflux called Barrett esophagus, tobacco use, obesity, and drinking alcohol. Symptoms are dysphagia, which slowly gets worse, and weight loss. In this procedure, a doctor looks down into your esophagus by passing a thin, lighted tube, through your mouth. It has a camera attached to it. The doctor can look at pictures of your digestive tract and can also take tissue samples biopsy of your esophagus to examine under a microscope.

Barium swallow. In this procedure, you swallow barium. This is a substance that coats the inside of your esophagus and shows up well on X-rays. Your doctor takes images of your esophagus. This test measures pressure inside your esophagus. It can tell your doctor if your peristalsis is normal. To change or withdraw your consent choices for VerywellHealth. At any time, you can update your settings through the "EU Privacy" link at the bottom of any page.

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