GI motility depends on the coordinated activity of circular and longitudinal smooth muscle (the tunica muscularis) in the walls of hollow GI organs. The proximal two-thirds of the oesophagus and the external anal sphincter contain skeletal muscle; the rest of the tunica muscularis is made of smooth muscle cells.
Smooth muscle cells are connected by gap junctions, which helps contractions spread and stay coordinated. The interstitial cells of Cajal are believed to generate spontaneous electrical impulses that spread to adjacent smooth muscle. In this sense, Cajal cells act as pacemakers of the GIT.
This spontaneous electrical activity does not require neuronal input and produces slow waves. Activation of Ca2±activated Cl− channels in Cajal cells generates inward currents, producing slow waves. Slow waves conduct to smooth muscle cells and create cycles of depolarization that can activate Ca2+ channels, allowing slow waves to couple to smooth muscle contractions. Slow-wave frequency varies from about 3/min in the stomach to about 12/min in the duodenum. The GIT shows both tonic (sustained) and phasic (transient) contractions.
Excitation-contraction coupling occurs when calcium enters through L-type calcium channels, causing depolarization. This is followed by opening of T-type calcium channels, which leads to further calcium influx. Ca2+ binding to calmodulin activates myosin light chain kinase, and phosphorylation of myosin initiates cross-bridge cycling. Myosin phosphatase dephosphorylates myosin to relax muscle, and Ca2+ sensitization regulates phosphatase activity.
Other channels, called TRP (transient receptor potential) channels, are voltage independent and nonselective for cations. Hormones and vagal stimulation can open additional nonselective cation channels, also causing depolarization. Repolarization occurs through opening of K+ channels. Intracellular Ca2+ levels, in turn, regulate the activity of these other channels.
Enteric neurons regulate the peristaltic reflex, segmentation movements, tonic contractions, and sphincter control.
Spontaneous pacemaker activity in the stomach, small intestine, and colon (electrical slow waves) organizes contractile patterns into phasic contractions that underlie peristaltic and segmental motility patterns. Basal slow-wave activity produces low-amplitude contractions, and inhibitory or excitatory neural inputs modulate contraction amplitude during each cycle.
Deglutition or swallowing: Swallowing has three phases - preparatory, transfer, and transport - that occur in sequence.
Anatomically, swallowing is divided into oral, pharyngeal, and esophageal phases. The oral phase includes the preparatory phase and the early transfer phase. The oral preparatory phase includes chewing, mixing food with saliva, and forming a bolus of suitable size and consistency.
As the bolus enters the esophagus, the esophagus, including the lower esophageal sphincter (LES), relaxes to receive it. Swallowing includes both voluntary and involuntary components: the preparatory/oral phase is voluntary, while the pharyngeal and esophageal phases are mediated by an involuntary swallowing reflex.
The muscles of the oral cavity and tongue are voluntary and striated. The muscles of the pharynx and cervical esophagus are specialized and striated, while the thoracic esophagus and LES are smooth muscle. The upper esophageal sphincter (UES) and LES are specialized sphincters that exhibit tonic contraction.
The striated muscles of the oral cavity, pharynx, and cervical esophagus are innervated by lower motor neurons carried in cranial nerves, including the vagus. These lower motor neurons are excitatory and stimulate striated muscle by releasing ACh at motor end plates.
The smooth muscle of the thoracic esophagus and LES is innervated by the vagus and the myenteric plexus. Autonomic innervation includes an excitatory pathway and a parallel inhibitory pathway: ACh is excitatory, while NO and VIP are inhibitory.
The swallowing center is located in the brainstem and innervates the motor nuclei of cranial nerves. Pharyngeal and esophageal peristalsis mediated by the swallowing reflex is called primary peristalsis.
The nucleus of the solitary tract sends fibers to the nucleus ambiguus of the vagus. Primary peristaltic movements are mediated by premotor neurons in the solitary tract, which project to the caudal and rostral parts of the dorsal motor nucleus of the vagus.
The inhibitory pathway neurons are activated first, inhibiting ongoing esophageal activity and relaxing the LES. This is followed by sequential activation of neurons to distal areas of the esophagus. Afferents in the superior laryngeal nerves are important stimulators of the swallowing reflex.
Esophageal peristalsis in the thoracic esophagus without an associated pharyngeal contraction is called secondary peristalsis. Its physiologic role is to clear the esophagus of food residues and refluxed material by moving them into the stomach. Secondary peristalsis is elicited by esophageal distention and is executed entirely by a local intramural reflex.
Transient LES relaxation, in which the LES relaxes without an associated peristaltic contraction reflex, has been implicated as an important mechanism of gastroesophageal reflux.
Small intestinal motility: Chyme is the semi-digested food that passes from the stomach into the duodenum. The small intestine shows two main types of contractions: segmentation and peristaltic contractions.
ACh and substance P stimulate movement, while VIP and NO cause relaxation. Sympathetic stimulation inhibits movement.
Large intestinal motility: Segmental contractions of the large intestine lead to haustra formation. Contraction of the ileocecal sphincter prevents reflux of contents into the ileum. Mass movements of the colon move colonic contents along the colon toward the rectum and occur 1-3 times per day. In the gastrocolic reflex, distension of the stomach increases mass movements.
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