The act of deglutition is a complex reflex activity. The initial phase is under voluntary control. Food is chewed, mixed with saliva and formed into an appropriately sized bolus before being thrust to the posterior pharynx by the tongue. Once the bolus reaches the posterior pharynx, receptors are activated that initiate the involuntary phase of deglutition. This involves the carefully sequenced contraction of myriad head and neck muscles. The food bolus is rapidly engulfed and pushed toward the esophagus by the pharyngeal constrictor muscles. Simultaneously there is activation of muscles that lift the palate and close off and elevate the larynx in order to prevent misdirection of the bolus. Almost immediately upon activation of this reflex, the UES opens just long enough to allow the food bolus to pass through; it then rapidly shuts to prevent retrograde passage of the bolus. The oropharyngeal phase is thus completed and the esophageal phase takes over. This involves two major phenomena: (1) the sequential contraction of the circular muscle of the esophageal body, which results in a contractile wave that migrates toward the stomach; and (2) the relaxation and opening of the LES, which allows the bolus to pass. The peristaltic sequence and associated UES and LES relaxation induced by swallowing are termed primary peristalsis. These can be assessed manometrically using an intraluminal tube to measure pressures. The typical sequence seen during primary peristalsis is depicted in Figure 1. Secondary peristalsis refers to a peristaltic sequence that occurs in response to distention of the esophagus. This is a localized peristaltic wave that usually begins just above the area of distention. It is associated with LES relaxation, but not with UES relaxation or deglutition.

The UES serves as a pressure barrier to prevent retrograde flow of esophageal contents and the entry of air into the esophagus during inspiration. This high-pressure zone is created by tonic contraction of the UES muscles, which is produced by tonic neuronal discharge of vagal lower motor neurons. With deglutition this neuronal discharge ceases temporarily and permits relaxation of the UES. UES opening will not occur with relaxation of the muscles alone; it requires elevation and anterior displacement of the larynx, which is mediated by contraction of the suprahyoid muscles. Relaxation lasts for only one second and is followed by a postrelaxation contraction (Figure 1).

There is a fundamental difference in the control mechanisms of peristalsis between the upper (striated-muscle) esophagus and the lower (smooth-muscle) esophagus. In the striated-muscle segment, peristalsis is produced by sequential firing of vagal lower motor neurons so that upper segments contract first and more aboral segments subsequently. In the smooth-muscle segment, the vagal preganglionic efferent fibers have some role in the aboral sequencing of contraction, but intrinsic neurons are also capable of evoking peristalsis independently of the extrinsic nervous system. Transection of vagal motor fibers to the esophagus in experimental animals will abolish primary peristalsis throughout the esophagus; however, in this setting, distention-induced or secondary peristalsis will be maintained in the smooth-muscle but not in the striated-muscle segment. Furthermore, if vagal efferent fibers are stimulated electrically (Figure 2), a simultaneous contraction will be produced in the striated-muscle esophagus that begins with the onset of the electrical stimulus, lasts throughout the stimulus, and ends abruptly when the stimulus is terminated. In the smooth-muscle esophagus, however, the response to vagal efferent nerve stimulation is quite different, in that the onset of contractions is delayed relative to the onset of the stimulus. The latency to onset of the contraction increases in the more distal segments of the esophagus (i.e., the evoked contractions are peristaltic).

This experimental observation indicates that intrinsic neuromuscular mechanisms exist and can mediate peristalsis on their own. Further evidence for this mechanism is found in studies where strips of esophageal circular smooth muscle are stimulated electrically in vitro. The latency to contraction after stimulation is shortest in the strips taken from the proximal smooth-muscle segment and increases progressively in the more distal strips.

This latency gradient of contraction is clearly important in the production of esophageal peristalsis. Although the exact mechanisms are unclear, initial or deglutitive inhibition is important. With primary or secondary peristalsis, a wave of neurally mediated inhibition initially spreads rapidly down the esophagus. This is caused by the release of a nonadrenergic, noncholinergic inhibitory neurotransmitter (most likely nitric oxide) that produces hyperpolarization (inhibition) of the circular smooth muscle. It is only after recovery from the initial hyperpolarization that esophageal muscle contraction (which is mediated primarily by cholinergic neurons) can occur. Thus, the duration of this initial inhibition is important with respect to the differential timing of the subsequent contraction. Derangements of the mechanisms behind this latency gradient lead to nonperistaltic contractions and dysphagia. Such derangements could result from problems with either the intrinsic neural mechanisms (enteric nervous system) or the central neuronal sequencing.

At the time of deglutition or when the esophagus is distended, the LES promptly relaxes. Swallow-induced LES relaxation is mediated by vagal efferent fibers that synapse on nonadrenergic, noncholinergic inhibitory neurons of the myenteric plexus. The inhibitory neurotransmitter released from these intrinsic neurons is probably nitric oxide. LES relaxation usually lasts about five to seven seconds, and is sufficient to abolish the gastroesophageal pressure barrier. This permits the food bolus to pass unimpeded from the esophagus to the stomach. The LES also relaxes to permit belching or vomiting. Inadequate LES relaxation is seen in achalasia and results in dysphagia.