Striated Muscle Portion Research Articles

ATP-Induced Contractile Response of Esophageal Smooth Muscle in Mice.

The tunica muscularis of mammalian esophagi is composed of striated muscle and smooth muscle. Contraction of the esophageal striated muscle portion is mainly controlled by cholinergic neurons. On the other hand, smooth muscle contraction and relaxation are controlled not only by cholinergic components but also by non-cholinergic components in the esophagus. Adenosine triphosphate (ATP) is known to regulate smooth muscle contraction and relaxation in the gastrointestinal tract via purinergic receptors. However, the precise mechanism of purinergic regulation in the esophagus is still unclear. Therefore, the aim of the present study was to clarify the effects of ATP on the mechanical responses of the esophageal muscle in mice. An isolated segment of the mouse esophagus was placed in a Magnus's tube and longitudinal mechanical responses were recorded. Exogenous application of ATP induced contractile responses in the esophageal preparations. Tetrodotoxin, a blocker of voltage-dependent sodium channels in neurons and striated muscle, did not affect the ATP-induced contraction. The ATP-evoked contraction was blocked by pretreatment with suramin, a purinergic receptor antagonist. RT-PCR revealed the expression of mRNA of purinergic receptor genes in the mouse esophageal tissue. The findings suggest that purinergic signaling might regulate the motor activity of mouse esophageal smooth muscle.

ATP-dependent potassium channels contribute to motor regulation of esophageal striated muscle in rats

The aim of the present study was to clarify roles of ATP-dependent potassium channels (KATP channels) in motility of the striated muscle portion in the esophagus. An isolated segment of the rat esophagus was placed in an organ bath and mechanical responses were recorded using a force transducer. Electrical stimulation of the vagus nerve evoked contractile response of striated muscle in the esophageal segment. Application of glibenclamide, an antagonist of KATP channels, increased amplitude of vagally mediated twitch contractions of the rat esophagus. On the other hand, minoxidil, an agonist of KATP channels, decreased amplitude of twitch contractions. RT-PCR revealed the expression of subunits of KATP channels in esophageal tissue. In addition, immunopositivity for subunits of KATP channels was observed in the striated muscle cells of the esophageal muscle layer. These findings indicate that KATP channels contribute to motor regulation of striated muscle in the rat esophagus.

Characterization of peristaltic motility in the striated muscle portion of the esophagus using a novel in vivo method in rats.

Esophageal peristalsis is controlled by the brainstem via vago-vagal reflex. However, the precise regulatory mechanisms in the striated muscle portion are largely unknown. The aim of this study was to characterize peristaltic motility in the portion of the esophagus using a novel in vivo method in rats. A balloon-tipped catheter was placed in the esophagus of a rat anesthetized with urethane. To induce esophageal peristalsis, the balloon was inflated by water injection. When the balloon was inflated near the bronchial bifurcation, the balloon was transported in the aboral direction. Vagotomy abolished the peristaltic response. The threshold volume for inducing esophageal peristalsis varied according to the velocity of balloon distention; the volume being effective to induce peristalsis at a low inflation speed was smaller than the threshold volume at a rapid inflation speed. Even in the absence of inflation, keeping the balloon inside the esophagus during an interval period prevented subsequent induction of peristaltic motility. In addition, a nitric oxide synthase inhibitor abolished the induction of esophageal peristalsis. Our findings suggest that (a) in addition to the intensity, the velocity of distention is important for activating the mechanosensory mechanism to induce esophageal peristalsis, (b) tonic inputs from afferent fibers located at the mucosa may reduce the excitability of mechanosensors which is necessary for inducing peristalsis, and (c) nitric oxide plays essential roles in the induction of esophageal peristalsis. These results provide novel insights into the regulatory mechanisms of esophageal motility.

Inhibitory actions of a local neural reflex on propulsive activity of the esophageal striated muscle portion in rats

The aim of the present study was to clarify functional roles of a local neural reflex in propulsive activity of the rat esophageal striated muscle. Firstly, we established a method for measuring the volume of fluid expelled from an isolated esophageal segment to evaluate propulsive activity. Electrical stimulation to vagus nerves induced propulsion of intraluminal solution in the esophageal segment. The vagally evoked propulsion was abolished in the presence of d-tubocurarine. Next, this quantitative method was applied to examine the functional roles of intrinsic nerves in the esophagus. Capsaicin, a stimulant of primary afferents, inhibited the vagally mediated propulsion. A nitric oxide synthase inhibitor or a selective tachykinin NK1 receptor antagonist significantly blocked the inhibitory effect of capsaicin. These findings suggest that the local neural reflex, which consists of tachykininergic and nitrergic neurons, might participate in modulation of propulsive activity in the striated muscle portion of the rat esophagus.

Modulatory mechanism of the striated muscle motility by a local neural reflex in the rat esophagus

The external muscle layers of the mammalian esophagus contain striated muscle fibers. These striated muscle fibers are innervated exclusively by excitatory vagal efferents and the peristalsis in the striated esophageal muscle is modulated via vago-vagal reflexes. By contrast, the presence of a distinct ganglionated myenteric plexus in the striated muscle portion of the mammalian esophagus has long been known. However, the role of the intrinsic nervous system in the peristalsis of the striated muscle portion of the esophagus has remained enigmatic, and has been neglected in terms of peristaltic control.

Central nervous system nitric oxide induces oropharyngeal swallowing and esophageal peristalsis in the cat

Background & Aims: The functional role of brainstem nitric oxide (NO) in swallowing and esophageal peristalsis remains unknown. We examined the effects of blockade of central nervous system (CNS) NO synthase (NOS) on swallowing and on primary and secondary peristalsis. Methods: (1) The effect of intravenous (IV) NOS inhibitor NG-nitro-L-arginine (L-NNA) on swallowing and swallowing-induced peristalsis was examined. (2) An NOS inhibitor (NG-monomethyl-L-arginine [L-NMMA]) was administered into the fourth ventricle intracerebroventricularly (ICV), and its effects on swallowing and primary and secondary peristalsis were examined. Results: (1) IV L-NNA significantly reduced the number of oropharyngeal swallows and the induction of primary peristalsis in the smooth muscle portion of the esophageal body; the change was not significant within the striated muscle portion. (2) L-NMMA given ICV significantly reduced the number of oropharyngeal swallows and the incidence of primary peristalsis in both smooth and striated muscle, but the reduction in amplitude was significant only for the smooth muscle contraction. There was a significant reduction in both the amplitude and incidence of secondary peristalsis, only in the smooth muscle portion. Conclusions: CNS NO is an important neurotransmitter in the induction of oropharyngeal swallowing and esophageal peristalsis. The neural substrates mediating striated and smooth muscle peristalsis may be both anatomically and neurochemically distinct.GASTROENTEROLOGY 2000;119:377-385

Proximal and distal esophageal contractions have similar manometric features.

The human esophagus is composed of striated muscle proximally and of smooth muscle distally with a transition zone between the two. Striated muscle contracts much faster than smooth muscle. The change in pressure over time (dP/dt) of the contraction amplitude should therefore be higher in proximal than in distal esophagus, reflecting the presence of striated muscle proximally. There were 34 normal esophageal manometries of patients analyzed for swallow amplitude and dP/dt in the pharynx and esophagus. An additional 11 healthy controls were similarly studied. Amplitudes in pharynx and proximal and distal esophagus were not different. The mid-esophagus had a pressure trough (P < 0.001). The dP/dt in the pharynx was much higher than that in the esophagus (P < 0.001). The dP/dt of proximal and distal esophagus were of the same order of magnitude. The manometric behavior of the striated muscle portion of the proximal esophagus differs from that seen in the pharynx and shows similar characteristics to distal esophageal smooth muscle.

Effect of adrenoceptor agonists on striated muscle strips of the canine oesophagus

1. Acute psychological stress, which could be related to the release of a large amount of catecholamines, may cause oesophageal motility disorders. Therefore, the aim of our study was to elucidate the influence of adrenoceptor agonists on the striated muscle portion of the oesophagus by use of isolated strips from dogs. 2. Contractions were evoked in isolated striated muscle strips by electrical field stimulation (1 pulse min-1, 1 ms/pulse, submaximal voltage). The effects induced by administration of adrenoceptor agonists alone or in the presence of antagonists were tested to determine the nature of the adrenoceptors on this muscle preparation. 3. The administration of both the natural adrenoceptor agonists, adrenaline and noradrenaline, and the synthetic beta-adrenoceptor agonists, isoprenaline (beta 1 + beta 2), dobutamine (beta 1) or ritodrine (beta 2), enhanced the amplitude of the contractions induced by electrical stimulation in a concentration-dependent manner. The maximum responses were 82.6 (adrenaline), 66.2 (noradrenaline), 86.2 (isoprenaline), 34.6 (dobutamine) and 80.8% (ritodrine). The EC20 values obtained were respectively 2 nM, 0.2 microM, 0.91 nM, 3 microM and 80 nM. The administration of the alpha 1-adrenoceptor agonist, phenylephrine, also enhanced the contractile response in a concentration-dependent manner (EC20 value = 0.3 microM) and the maximum response was 64.6%, but the administration of the alpha 2-adrenoceptor agonist, clonidine, did not influence the contractile response. These data suggest the involvement of beta 2- and possibly alpha 1-adrenoceptors in the responses of these adrenoceptor agonists. 4 The selective P2-adrenoceptor antagonist ICI 118551 (3-100nM) shifted the concentration-effect curves for noradrenaline, phenylephrine and ritodrine to the right in a concentration-dependent manner.ICI 118551 (3 nM) also shifted the concentration-effect curves for adrenaline and isoprenaline to the right, but increasing the concentration of ICI 118551 did not cause any further antagonist activity until a concentration of 100 nM, when a further rightward shift was obtained.5. The selective alpha 1-adrenoceptor antagonist, prazosin (30-300 nM), did not affect the increased contractile responses induced by adrenaline, noradrenaline, phenylephrine, isoprenaline or ritodrine.6. In conclusion, it appears that beta2-adrenoceptors are present in the striated muscle portion of the canine oesophagus, where they mediate an enhancement of contractile responses evoked by electrical stimulation. The alpha l-agonist, phenylephrine, appears to interact with beta2-adrenoceptors on this preparation.beta 3-Adrenoceptors have already been demonstrated in smooth muscle from various parts of the gastrointestinal tract, and our study does not exclude the possibility that there is an additional population of beta 3-receptors in the canine striated muscle part of the oesophagus.

Nicotine stimulates esophageal peristaltic contractions in cats by a central mechanism.

The aim of the present study was to 1) characterize nicotine-induced peristalsis in the feline esophagus and 2) determine the site of action of nicotine. Experiments were done on ketamine-sedated cats. Esophageal contractions were measured using a multilumen catheter assembly system. After recording 1 degree and 2 degrees peristaltic sequences nicotine (50-100 micrograms/kg iv) was administered. Nicotine induced a peristaltic contraction through the esophageal striated and smooth muscle part of the esophagus, which was not associated with any mylohyoid electromyogram activity or pharyngeal response, although the upper esophageal sphincter did relax. Addition of either atropine (20-50 micrograms/kg iv) or hexamethonium (10-20 mg/kg iv), a peripherally acting nicotinic antagonist, did not affect the striated muscle portion of the nicotine-induced esophageal contractile response but antagonized the smooth muscle response. However, mecamylamine (0.5-1 mg/kg iv), a ganglionic antagonist that crosses the blood-brain barrier, abolished the esophageal response to nicotine. Succinylcholine (0.5-1 mg/kg iv) abolished the striated muscle response without affecting the nicotine-induced smooth muscle contractility. Finally, the nicotine-induced peristaltic sequence was abolished after bilateral cervical vagotomy. In conclusion, nicotine, administered peripherally, activates central brain stem mechanisms that mediate a peristaltic sequence through the feline esophagus.

Effect of Acute Ethanol on Esophageal Motility in Cat

In man, acute ethanol administration decreases lower esophageal sphincter pressure (LESP), prolongs the duration, and lowers the amplitude of esophageal contractions. These changes may contribute to gastroesophageal reflux and esophagitis. To evaluate the underlying mechanisms of these changes an animal model is needed. Hence, we studied the effect of various doses of ethanol on esophageal motility in cats, an animal with an esophagus similar to man's. Similar to man, intravenous administration of ethanol significantly decreased LESP and amplitude of lower (smooth muscle portion) esophageal contractions. It also prolonged the duration of lower esophageal contractions, even through it had no effect on contraction velocity. The effect of ethanol on upper (striated muscle portion) esophagus was different. Ethanol had no effect on the amplitude of contractions, whereas it prolonged their duration and decreased their velocity. The effect of acute ethanol on LESP in four withdrawing alcoholic cats was similar to controls. However, the acute effect of ethanol on the esophageal contractions was less marked in alcoholics. Bilateral cervical vagotomy and intravenous injection of the neurotoxin tetrodotoxin before the administration of ethanol did not prevent the effect of ethanol on LESP. This data suggests that cat esophagus is a good model for studying the underlying mechanisms of the effects of acute ethanol because its response is similar to the esophagus of man, and the acute effect of ethanol on LESP is not neurally mediated but is the result of its direct effect on muscle.

Central nervous system lymphoma presenting as dysphagia

Two patients are presented having lymphomatous involvement of the central nervous system in whom dysphagia was the predominant symptom. All indicated studies failed to reveal evidence of direct esophageal involvement, and the dysphagia improved during treatment of the neural component. Esophageal manometric studies revealed abnormalities of the striated muscle portion of the esophagus. These two case histories suggest that invasion of the central nervous system with lymphoma may produce abnormalities of the neuromuscular control of esophageal function resulting in dysphagia.

Necessity of a bolus for propagation of primary peristalsis in the canine esophagus.

ARTICLESNecessity of a bolus for propagation of primary peristalsis in the canine esophagusEH Longhi, and Jordan PH JrEH Longhi, and Jordan PH JrPublished Online:01 Mar 1971https://doi.org/10.1152/ajplegacy.1971.220.3.609MoreSectionsPDF (875 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByFunctional Anatomy and Physiology of Swallowing and Esophageal Motility30 April 2021Characterization of peristaltic motility in the striated muscle portion of the esophagus using a novel in vivo method in rats14 December 2018 | Neurogastroenterology & Motility, Vol. 31, No. 4Role of peripheral reflexes in the initiation of the esophageal phase of swallowingIvan M. Lang, Bidyut K. Medda, Arash Babaei, and Reza Shaker15 April 2014 | American Journal of Physiology-Gastrointestinal and Liver Physiology, Vol. 306, No. 8Esophageal Motor Physiology25 July 2012Functional Anatomy and Physiology of Swallowing and Esophageal Motility28 March 2012Brain Stem Control of the Phases of Swallowing28 April 2009 | Dysphagia, Vol. 24, No. 3Pharyngeal Swallowing: Defining Pharyngeal and Upper Esophageal Sphincter Relationships in Human NeonatesThe Journal of Pediatrics, Vol. 151, No. 6Mechanisms of reflexes induced by esophageal distensionIvan M. Lang, Bidyut K. Medda, and Reza Shaker1 November 2001 | American Journal of Physiology-Gastrointestinal and Liver Physiology, Vol. 281, No. 5Brain Stem Control of Swallowing: Neuronal Network and Cellular MechanismsAndré Jean1 April 2001 | Physiological Reviews, Vol. 81, No. 2Central nervous system nitric oxide induces oropharyngeal swallowing and esophageal peristalsis in the catGastroenterology, Vol. 119, No. 2Vagal afferent dysfunction in naturally occurring canine esophageal motility disorderDigestive Diseases and Sciences, Vol. 39, No. 10Oesophageal compliance in naturally occurring canine megaoesophagusAustralian Veterinary Journal, Vol. 70, No. 11Central neural control of esophageal motility: A reviewDysphagia, Vol. 5, No. 1In vivo myoelectric activity: methods, analysis, and interpretation1 January 2011Esophageal motility1 January 2011Adaptation to surgical perturbations1 January 2011Assessment of the neural defect in a dog with idiopathic megaesophagusDigestive Diseases and Sciences, Vol. 32, No. 1Neurophysiological basis of swallowingDysphagia, Vol. 1, No. 2The origins of innervation of the esophagus of the dogBrain Research, Vol. 326, No. 1Control of the central swallowing program by inputs from the peripheral receptors. A reviewJournal of the Autonomic Nervous System, Vol. 10, No. 3-4Normal Swallowing in the Dog: A Cineradiographic Study19 May 2005 | Veterinary Radiology, Vol. 20, No. 3-6Motor innervation of striated oesophageal muscleJournal of the Neurological Sciences, Vol. 36, No. 2Myogenic and Neural Control Systems for Esophageal MotilityGastroenterology, Vol. 73, No. 6Neural Control Of Esophageal PeristalsisGastroenterology, Vol. 72, No. 3Peristalsis in Smooth Muscle Esophagus After Transection and Bolus DeviationGastroenterology, Vol. 71, No. 6Physiologie des tubulären OesophagusNeural Organization of Esophageal Peristalsis: Role of Vagus NerveGastroenterology, Vol. 68, No. 3Congenital Atresia of the Oesophagus:A Follow-up Study in 36 Surgically Corrected Cases12 July 2009 | Scandinavian Journal of Thoracic and Cardiovascular Surgery, Vol. 9, No. 1Studies on the Necessity of a Bolus for the Progression of Secondary Peristalsis in the Canine EsophagusGastroenterology, Vol. 67, No. 2PhysiologyIs the Primary Peristaltic Contraction of the Canine Esophagus Bolus-Dependent?Gastroenterology, Vol. 65, No. 5Manometric Characteristics of Idiopathic Megaesophagus in the Dog: An Unsuitable Animal Model for Achalasia in ManGastroenterology, Vol. 65, No. 2 More from this issue > Volume 220Issue 3March 1971Pages 609-612 Copyright & PermissionsCopyright © 1971 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1971.220.3.609PubMed5545667History Published online 1 March 1971 Published in print 1 March 1971 Metrics