Vagal control of nitric oxide and vasoactive intestinal polypeptide release in the regulation of gastric relaxation in rat.

Takahashi, Toshio; Owyang, Chung

doi:10.1113/jphysiol.1995.sp020680

Cited by 128 publications

(107 citation statements)

References 45 publications

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“…The data presented here illustrate that L-glutamate microinjected into the caudal DMN evokes gastric relaxation. This response probably mediated cholinergic preganglionic neurons that synapse onto postganglionic/enteric NANC motor inhibitory neurons (21). If orexin A were activating postsynaptic OR1 on vagal preganglionic motor neurons in the caudal DMN, then inhibition of gastric motor function would be predicted.…”

Section: Discussionmentioning

confidence: 99%

Orexins in rat dorsal motor nucleus of the vagus potently stimulate gastric motor function

Krowicki

Burmeister

Berthoud

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

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. Orexins in rat dorsal motor nucleus of the vagus potently stimulate gastric motor function. Am J Physiol Gastrointest Liver Physiol 283: G465-G472, 2002. First published October 10, 2001 10.1152/ajpgi.00264.2001.-Orexins regulate food intake, arousal, and the sleep-wake cycle. They are synthesized by neurons in the lateral hypothalamus and project to autonomic areas in the hindbrain. Orexin A applied to the dorsal surface of the medulla stimulates gastric acid secretion via a vagally mediated pathway. We tested the hypothesis that orexins in the dorsal motor nucleus (DMN) of the vagus regulate gastric motor function. Multibarelled micropipette assemblies were used to administer vehicle, L-glutamate, orexins A (1 and 10 pmol) and B (10 pmol), and a dye marker into this site in anesthetized rats. When the pipette was positioned in the DMN rostral to the obex (where excitation of neurons by L-glutamate evoked an increase in contractility), orexins A and B increased intragastric pressure and antral motility. In contrast, 10 pmol orexin A microinjected into the DMN caudal to the obex (where L-glutamate evokes gastric relaxation through a vagal inhibitory pathway) did not significantly alter gastric motor function. In separate immunocytochemical studies, orexin receptor 1 was highly expressed in neurons in the DMN. Specifically, it was present in retrogradely labeled preganglionic neurons in the DMN that innervate the stomach. These data are consistent with the idea that orexin A stimulates vagal excitatory motor neurons. These are the first data to suggest that orexins in the DMN have potent and long-lasting effects to increase gastric contractility.brain-gut, hindbrain, gastrointestinal, feeding, motility OREXINS ARE NOVEL PEPTIDES that are synthesized exclusively by neurons in the lateral hypothalamic area (17). This single population of neurons supplies a widespread distribution of orexins in the brain (12, 13). There are two forms, orexins A and B (also known as hypocretin1 and hypocretin 2), which have affinity for orexin receptors 1 (OR1) and 2 (OR2), respectively.Orexins are thought to be involved in diverse functions, such as the regulation of the sleep-wake cycle, pain, and arousal; however, many studies have emphasized their role in energy homeostasis. For example, orexin A stimulates feeding when applied to regions of the hypothalamus (5). Orexins of hypothalamic origin have been linked to the dorsal vagal complex (see below). This is where they could integrate energy balance homeostasis with sensory information from the viscera and bloodstream. The vagus nerve conveys both descending influences that prepare and coordinate the gut to receive food and sensory feedback from the gastrointestinal tract about meal size and composition. Integration of vagal afferent-efferent pathways from the gut occurs at the level of the dorsal vagal complex of the hindbrain medulla. This complex comprises the dorsal motor nucleus (DMN) of the vagus, where preganglionic motor neurons innervating the gastrointestinal tract a...

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Section: Discussionmentioning

confidence: 99%

Orexins in rat dorsal motor nucleus of the vagus potently stimulate gastric motor function

Krowicki

Burmeister

Berthoud

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…CCK-8s was injected into the DVC as described above. Drug doses were chosen based on previously published data (67)(68)(69)74) or were extrapolated from in vitro stud ies (4,7).…”

Section: Methodsmentioning

confidence: 99%

Effects of brain stem cholecystokinin-8s on gastric tone and esophageal-gastric reflex

Holmes¹,

Tong²,

Travagli³

2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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Holmes GM, Tong M, Travagli RA. Effects of brain stem cholecystokinin-8s on gastric tone and esophageal-gastric reflex. Am J Physiol Gastrointest Liver Physiol 296: G621-G631, 2009. First published January 8, 2009 doi:10.1152/ajpgi.90567.2008.-The actions of cholecystokinin (CCK) on gastrointestinal functions occur mainly via paracrine effects on peripheral sensory vagal fibers, which engage vago-vagal brain stem circuits to convey effector responses back to the gastrointestinal tract. Recent evidence suggests, however, that CCK also affects brain stem structures directly. Many electrophysiological studies, including our own, have shown that brain stem vagal circuits are excited by sulfated CCK (CCK-8s) directly, and we have further demonstrated that CCK-8s induces a remarkable degree of plasticity in GABAergic brain stem synapses. In the present study, we used fasted, anesthetized Sprague-Dawley rats to investigate the effects of brain stem administration of CCK-8s on gastric tone before and after activation of the esophageal-gastric reflex. CCK-8s microinjected in the dorsal vagal complex (DVC) or applied on the floor of the fourth ventricle induced an immediate and transient decrease in gastric tone. Upon recovery of gastric tone to baseline values, the gastric relaxation induced by esophageal distension was attenuated or even reversed. The effects of CCK-8s were antagonized by vagotomy or fourth ventricular, but not intravenous, administration of the CCK-A antagonist lorglumide, suggesting a central, not peripheral, site of action. The gastric relaxation induced by DVC microinjection of CCK-8s was unaffected by pretreatment with systemic bethanecol but was completely blocked by N G -nitro-L-arginine methyl ester, suggesting a nitrergic mechanism of action. These data suggest that 1) brain stem application of CCK-8s induces a vagally mediated gastric relaxation; 2) the CCK-8s-induced gastric relaxation is mediated via activation of nonadrenergic, noncholinergic pathways; and 3) CCK-8s reverses the esophageal-gastric reflex transiently.vago-vagal reflexes; gastric reflexes ESOPHAGEAL DISTENSION has long been recognized to elicit a robust and reflexive gastric relaxation (21). Early models of gastrointestinal vago-vagal reflexes presented a framework to explain many of the features of the brain stem circuits devoted to gastric reflex control, whereby stimulation of sensory vagal afferent fibers activates second-order neurons of the nucleus tractus solitarii (NTS). Subsequently, these second-order neurons modulate the output of preganglionic neurons in the dorsal motor nucleus of the vagus (DMV) that, in turn, control gastric functions to complete the vago-vagal loop (reviewed in Ref. 72).The esophageal-gastric reflex (or receptive relaxation) decreases gastric tone and allows swallowed food to be transported to the stomach with a minimal increase in intragastric pressure. Neurophysiological studies by Jean first showed the association of neurons of the caudal brain stem with esophageal function (reviewed in Re...

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“…The releasing of biologically active substances from nerve afferents provides gastro-protection by increasing blood flow and reducing acid secretion. This effect is associated with stimulation of CGRP receptors type 1 of smooth muscle cells and arteriole endothelium, which leads to activation of ATP-sensitive K + channels, increased production of nitric oxide and prostaglandins [23]. Similarly, afferent activation in duodenum over the low luminal pH leads to the inclusion of local reflexes and serotonin release, which induces increased НСО 3 -secretion.…”

Section: Role Of Afferent Nerves In Gastroduodenal Adaptationmentioning

confidence: 99%

Role of Vagus Nerve in Gastroduodenal Adaptation and Cytoprotection

Sulaieva¹,

Obraztsova²

2014

AJCEM

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Abstract:Objective: In this review we focused on understanding the cause-and-effect relationships of gastroduodenal pathology aiming to clarify the role of vagus nerve. Results: The spectrum of vagus nerve biological effects in gastroduodenal area is related to its numerous targets and a wide range of its receptors. A variety of vagus nerve effects are related to the broad expression of cholinergic receptors on the target cells: smooth muscle cells, covering and glandular epithelium of stomach and duodenum, myofibroblasts and mast cells, vascular endothelium, intramural ganglion neurons, endocrine cells, platelets and blood leukocytes. In this paper, we discussed the following issues: 1) role of sensory nerve endings in the vagal reflex regulation; 2) impact of gastrin and leptin on vagal afferentation; 3) targets of vagus efferent nerves; 4) the role of acetylcholine in regulation of functional activity of oxyntic cells; 5) relationship of vagus efferents with enteroendocrine cells; 6) the role of vagus nerve in realization of compensatory and adaptive reactions in gastroduodenal area. Conclusion: Vagus nerve is one of the key regulators of mucosal activity and blood supply, modulating adaptive reactions and maintaining the gastrointestinal barrier. Keywords: Gastroduodenal Area, Vagus Nerve, Afferent and Efferent NervesGastrointestinal pathology takes one of the leading places in the morbidity rate. A long-time comprehensive study has helped in determining the spectrum of exogenous and endogenous pathological factors that are associated with gastroduodenal pathology. It can be stated, that issues of digestive system regulation has been in focus of scientist for more than two centuries [1]. Nevertheless, pathogenesis of such disorders as gastroesophageal reflux disease, gastritis, peptic ulcer disease, duodenitis is still not clear.Structural homeostasis and functions of gastroduodenal area (GDA) are controlled by neural link, specific gastrointestinal regulatory peptides that have endo-, paraand neuroendocrine effects; and local factors -cytokines, growth factors, nitric oxide, etc. [2-3]. These regulatory molecules are produced by various cells of the mucosa and neurons of intramural ganglia. The auto-regulation, synchronicity, sequence, integration and protection of digestive organs are achieved due to the potentiation and modulation of these molecules [4,5]. At the same time there is a hierarchy of GDA regulatory mechanisms, due to which any disorder automatically activates higher levels of management and control, that's why neuro-endocrine control goes on the forefront [3,6]. Initially, the centers of autonomic nervous systems are activated that leads us to the aim of this review to fully analyze the structural organization of the parasympathetic innervation and role of vagus nerve in the pathology and compensatory-adaptive processes in GDA.Vagus nerve dependent gastric reflexes are mediated through vagal afferent fibers synapsing upon neurons of the nucleus tractus solitarius which, in turn, modulates the...

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Vagal control of nitric oxide and vasoactive intestinal polypeptide release in the regulation of gastric relaxation in rat.

Cited by 128 publications

References 45 publications

Orexins in rat dorsal motor nucleus of the vagus potently stimulate gastric motor function

Orexins in rat dorsal motor nucleus of the vagus potently stimulate gastric motor function

Effects of brain stem cholecystokinin-8s on gastric tone and esophageal-gastric reflex

Role of Vagus Nerve in Gastroduodenal Adaptation and Cytoprotection

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