The Experts below are selected from a list of 192 Experts worldwide ranked by ideXlab platform
Richard C. Rogers - One of the best experts on this subject based on the ideXlab platform.
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proteinase activated receptors in the nucleus of the solitary tract evidence for glial neural interactions in autonomic control of the stomach
The Journal of Neuroscience, 2009Co-Authors: Gerlinda E. Hermann, Montina J Van Meter, Jennifer Rood, Richard C. RogersAbstract:Bleeding head injury is associated with gastric stasis, a symptom of collapse of autonomic control of the gut described by Cushing around 1932. Recent work suggests that the proteinase thrombin, produced secondary to bleeding, may be the root cause. Results from our in vivo physiological studies show that fourth ventricular injection of PAR1 agonists, as well as thrombin itself, produced significant reductions in gastric transit in the awake rat. We expected that the PAR1 effect to inhibit gastric transit was the result of direct action on Vagovagal Reflex circuitry in the dorsal medulla. Surprisingly, our immunohistochemical studies demonstrated that PAR1 receptors are localized exclusively to the astrocytes and not the neurons in the nucleus of the solitary tract (NST; principal locus integrating visceral afferent input and part of the gastric Vagovagal Reflex control circuitry). Our in vitro calcium imaging studies of hindbrain slices revealed that PAR1 activation initially causes a dramatic increase in astrocytic calcium, followed seconds later by an increase in calcium signal in NST neurons. The neuronal effect, but not the astrocytic effect, of PAR1 activation was eliminated by glutamate receptor antagonism. TTX did not eliminate the effects of PAR1 activation on either glia or neurons. Thus, we propose that glia are the primary CNS sensors for PAR agonists and that the response of these glial cells drives the activity of adjacent (e.g., NST) neurons. These results show, for the first time, that changes in autonomic control can be directly signaled by glial detection of local chemical stimuli.
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Comments on “Hindbrain chemical mediators of Reflex-induced inhibition of gastric tone produced by esophageal distension and intravenous nicotine”
American Journal of Physiology-Regulatory Integrative and Comparative Physiology, 2006Co-Authors: Richard C. Rogers, Gerlinda E. Hermann, R. Alberto TravagliAbstract:The purpose of this study was to activate a Vagovagal Reflex by using esophageal distension and nicotine and test whether hindbrain nitric oxide and norepinephrine are involved in this Reflex function. We used double-labeling immunocytochemical methods to determine whether esophageal distension (and nicotine) activates c-Fos expression in nitrergic and noradrenergic neurons in the nucleus tractus solitarii (NTS). We also studied c-Fos expression in the dorsal motor nucleus of the vagus (DMV) neurons projecting to the periphery. Esophageal distension caused 19.7 ± 2.3% of the noradrenergic NTS neurons located 0.60 mm rostral to the calamus scriptorius (CS) to be activated but had little effect on c-Fos in DMV neurons. Intravenous administration of nicotine caused 19.7 ± 4.2% of the noradrenergic NTS neurons 0.90 mm rostral to CS to be activated and, as reported previously, had no effect on c-Fos expression in DMV neurons. To determine whether norepinephrine and nitric oxide were central mediators of esophageal distension-induced decrease in intragastric pressure (balloon recording), N G-nitro-l-arginine methyl ester microinjected into the NTS ( n = 5), but not into the DMV, blocked the Vagovagal Reflex. Conversely, α2-adrenergic blockers microinjected into the DMV ( n = 7), but not into the NTS, blocked the Vagovagal Reflex. These data, in combination with our earlier pharmacological microinjection data with nicotine, indicate that both esophageal distension and nicotine produce nitric oxide in the NTS, which then activates noradrenergic neurons that terminate on and inhibit DMV neurons.
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Central inhibitory action of peptide YY on gastric motility in rats.
American Journal of Physiology-Regulatory Integrative and Comparative Physiology, 1995Co-Authors: Chi-hsiang Chen, Richard C. RogersAbstract:Specific peptide YY (PYY) binding sites have recently been identified autoradiographically in the area postrema, nucleus of the solitary tract, and dorsal motor nucleus regions [collectively referred to as the dorsal vagal complex (DVC)] in rats. These medullary brain stem regions are responsible for Vagovagal Reflex control of gastric function, including gastric motility. We propose that PYY can modulate gastrointestinal functions, such as gastric motility, by interacting with PYY binding sites found in DVC. Furthermore, we predict that central PYY effects on gastric function are mediated by the vagus nerve. In the present study, urethan-anesthetized rats were used. PYY (20.0 and 2.0 fmol) injected directly into DVCs of the animals produced significant inhibition of gastric motility that was stimulated by centrally applied thyrotropin-releasing hormone (TRH). TRH is a well-accepted central stimulator of vagal efferent pathway to the stomach. Otherwise, an excitatory effect of PYY (2 pmol) on basal gastric motility was observed and considered as being pharmacological. The inhibitory effect of PYY was abolished completely by unilateral (the injection side) cervical vagotomy, suggesting that the inhibition was vagally dependent. These results support the view that physiological concentrations of PYY may inhibit proximal gut function as part of the “ileal brake” mechanism by acting directly on Vagovagal control circuits in the dorsal medulla. However, extremely high doses of PYY may activate gastric function through pharmacological action at pancreatic polypeptide receptors in the DVC.
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Vagovagal Reflex control of digestion: afferent modulation by neural and "endoneurocrine" factors
American Journal of Physiology-Gastrointestinal and Liver Physiology, 1995Co-Authors: Richard C. Rogers, Dana M. Mctigue, Gerlinda E. HermannAbstract:Vagovagal Reflex control circuits in the dorsal vagal complex of the brain stem provide overall coordination of gastric, small intestinal, and pancreatic digestive functions. The neural components forming these Reflex circuits are under substantial descending neural control. By adjusting the excitability of the differing components of the Reflex, significant alterations in digestion control can be produced by the central nervous system. Additionally, the dorsal vagal complex is situated within a circumventricular region without a "blood-brain barrier." As a result, Vagovagal Reflex circuitry is also exposed to humoral influences, which can profoundly alter digestive functions by acting directly on brain stem neurons.
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Pancreatic polypeptide in dorsal vagal complex stimulates gastric acid secretion and motility in rats
American Journal of Physiology-gastrointestinal and Liver Physiology, 1993Co-Authors: Dana M. Mctigue, N. K. Edwards, Richard C. RogersAbstract:High concentrations of receptors for pancreatic polypeptide (PP), a pancreatic hormone, were recently discovered in the dorsomedial region of the dorsal vagal complex (DVC). We hypothesized that gastric acid secretion and motility, digestive functions strongly influenced by Vagovagal Reflexes organized within the DVC, would be affected by PP applied directly to this vagal sensorimotor integration area. After urethan-anesthetized rats were prepared for antral motility recording or titrometric analysis of gastric acid output, phosphate-buffered saline or various doses of PP in phosphate-buffered saline were micropressure injected into the medial DVC. Injections of PP into the DVC produced significant, long-lasting, and dose-dependent increases in gastric acid secretion and antral motility. These gastric responses were blocked by bilateral cervical vagotomy and by atropine, suggesting that intramedullary PP stimulates vagal cholinergic pathways, resulting in enhanced gastric functions. Because PP is not synthesized within the central nervous system, these results point to a new mechanism whereby the digestive tract may modulate its own autonomic control: direct humoral action on Vagovagal Reflex circuits within the brain stem.
Laura Anselmi - One of the best experts on this subject based on the ideXlab platform.
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Vagal neurocircuitry and its influence on gastric motility
Nature Reviews Gastroenterology & Hepatology, 2016Co-Authors: R. Alberto Travagli, Laura AnselmiAbstract:Upper gastrointestinal tract function is regulated by Vagovagal neurocircuits, comprising brainstem nuclei that integrate visceral sensory information and provide vagal motor output. Here, Travagli and Anselmi describe the organization of these neurocircuits and their plasticity in response to stressors. The influence of gastrointestinal peptides on Vagovagal neurons is also discussed. A large body of research has been dedicated to the effects of gastrointestinal peptides on vagal afferent fibres, yet multiple lines of evidence indicate that gastrointestinal peptides also modulate brainstem vagal neurocircuitry, and that this modulation has a fundamental role in the physiology and pathophysiology of the upper gastrointestinal tract. In fact, brainstem Vagovagal neurocircuits comprise highly plastic neurons and synapses connecting afferent vagal fibres, second order neurons of the nucleus tractus solitarius (NTS), and efferent fibres originating in the dorsal motor nucleus of the vagus (DMV). Neuronal communication between the NTS and DMV is regulated by the presence of a variety of inputs, both from within the brainstem itself as well as from higher centres, which utilize an array of neurotransmitters and neuromodulators. Because of the circumventricular nature of these brainstem areas, circulating hormones can also modulate the vagal output to the upper gastrointestinal tract. This Review summarizes the organization and function of Vagovagal Reflex control of the upper gastrointestinal tract, presents data on the plasticity within these neurocircuits after stress, and discusses the gastrointestinal dysfunctions observed in Parkinson disease as examples of physiological adjustment and maladaptation of these Reflexes. Brainstem Vagovagal neurocircuits modulate the functions of the upper gastrointestinal tract Neuronal communications between vagal sensory (nucleus tractus solitarius, NTS) and motor (dorsal motor nucleus of the vagus, DMV) nuclei are highly specialized and probably specific for function and target organ NTS–DMV synaptic contacts are not static but undergo plastic changes to ensure that vagally regulated gastrointestinal functions respond appropriately to ever-changing physiological conditions or derangements Gastrointestinal peptides influence Vagovagal circuits via actions on both vagal afferent fibres and brainstem nuclei Neurodegenerative alterations of the vagal neurocircuitry induce marked impairments of gastrointestinal functions
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Vagal neurocircuitry and its influence on gastric motility.
Nature Reviews Gastroenterology & Hepatology, 2016Co-Authors: R. Alberto Travagli, Laura AnselmiAbstract:A large body of research has been dedicated to the effects of gastrointestinal peptides on vagal afferent fibres, yet multiple lines of evidence indicate that gastrointestinal peptides also modulate brainstem vagal neurocircuitry, and that this modulation has a fundamental role in the physiology and pathophysiology of the upper gastrointestinal tract. In fact, brainstem Vagovagal neurocircuits comprise highly plastic neurons and synapses connecting afferent vagal fibres, second order neurons of the nucleus tractus solitarius (NTS), and efferent fibres originating in the dorsal motor nucleus of the vagus (DMV). Neuronal communication between the NTS and DMV is regulated by the presence of a variety of inputs, both from within the brainstem itself as well as from higher centres, which utilize an array of neurotransmitters and neuromodulators. Because of the circumventricular nature of these brainstem areas, circulating hormones can also modulate the vagal output to the upper gastrointestinal tract. This Review summarizes the organization and function of Vagovagal Reflex control of the upper gastrointestinal tract, presents data on the plasticity within these neurocircuits after stress, and discusses the gastrointestinal dysfunctions observed in Parkinson disease as examples of physiological adjustment and maladaptation of these Reflexes.
R. Alberto Travagli - One of the best experts on this subject based on the ideXlab platform.
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Vagal neurocircuitry and its influence on gastric motility
Nature Reviews Gastroenterology & Hepatology, 2016Co-Authors: R. Alberto Travagli, Laura AnselmiAbstract:Upper gastrointestinal tract function is regulated by Vagovagal neurocircuits, comprising brainstem nuclei that integrate visceral sensory information and provide vagal motor output. Here, Travagli and Anselmi describe the organization of these neurocircuits and their plasticity in response to stressors. The influence of gastrointestinal peptides on Vagovagal neurons is also discussed. A large body of research has been dedicated to the effects of gastrointestinal peptides on vagal afferent fibres, yet multiple lines of evidence indicate that gastrointestinal peptides also modulate brainstem vagal neurocircuitry, and that this modulation has a fundamental role in the physiology and pathophysiology of the upper gastrointestinal tract. In fact, brainstem Vagovagal neurocircuits comprise highly plastic neurons and synapses connecting afferent vagal fibres, second order neurons of the nucleus tractus solitarius (NTS), and efferent fibres originating in the dorsal motor nucleus of the vagus (DMV). Neuronal communication between the NTS and DMV is regulated by the presence of a variety of inputs, both from within the brainstem itself as well as from higher centres, which utilize an array of neurotransmitters and neuromodulators. Because of the circumventricular nature of these brainstem areas, circulating hormones can also modulate the vagal output to the upper gastrointestinal tract. This Review summarizes the organization and function of Vagovagal Reflex control of the upper gastrointestinal tract, presents data on the plasticity within these neurocircuits after stress, and discusses the gastrointestinal dysfunctions observed in Parkinson disease as examples of physiological adjustment and maladaptation of these Reflexes. Brainstem Vagovagal neurocircuits modulate the functions of the upper gastrointestinal tract Neuronal communications between vagal sensory (nucleus tractus solitarius, NTS) and motor (dorsal motor nucleus of the vagus, DMV) nuclei are highly specialized and probably specific for function and target organ NTS–DMV synaptic contacts are not static but undergo plastic changes to ensure that vagally regulated gastrointestinal functions respond appropriately to ever-changing physiological conditions or derangements Gastrointestinal peptides influence Vagovagal circuits via actions on both vagal afferent fibres and brainstem nuclei Neurodegenerative alterations of the vagal neurocircuitry induce marked impairments of gastrointestinal functions
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Vagal neurocircuitry and its influence on gastric motility.
Nature Reviews Gastroenterology & Hepatology, 2016Co-Authors: R. Alberto Travagli, Laura AnselmiAbstract:A large body of research has been dedicated to the effects of gastrointestinal peptides on vagal afferent fibres, yet multiple lines of evidence indicate that gastrointestinal peptides also modulate brainstem vagal neurocircuitry, and that this modulation has a fundamental role in the physiology and pathophysiology of the upper gastrointestinal tract. In fact, brainstem Vagovagal neurocircuits comprise highly plastic neurons and synapses connecting afferent vagal fibres, second order neurons of the nucleus tractus solitarius (NTS), and efferent fibres originating in the dorsal motor nucleus of the vagus (DMV). Neuronal communication between the NTS and DMV is regulated by the presence of a variety of inputs, both from within the brainstem itself as well as from higher centres, which utilize an array of neurotransmitters and neuromodulators. Because of the circumventricular nature of these brainstem areas, circulating hormones can also modulate the vagal output to the upper gastrointestinal tract. This Review summarizes the organization and function of Vagovagal Reflex control of the upper gastrointestinal tract, presents data on the plasticity within these neurocircuits after stress, and discusses the gastrointestinal dysfunctions observed in Parkinson disease as examples of physiological adjustment and maladaptation of these Reflexes.
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Comments on “Hindbrain chemical mediators of Reflex-induced inhibition of gastric tone produced by esophageal distension and intravenous nicotine”
American Journal of Physiology-Regulatory Integrative and Comparative Physiology, 2006Co-Authors: Richard C. Rogers, Gerlinda E. Hermann, R. Alberto TravagliAbstract:The purpose of this study was to activate a Vagovagal Reflex by using esophageal distension and nicotine and test whether hindbrain nitric oxide and norepinephrine are involved in this Reflex function. We used double-labeling immunocytochemical methods to determine whether esophageal distension (and nicotine) activates c-Fos expression in nitrergic and noradrenergic neurons in the nucleus tractus solitarii (NTS). We also studied c-Fos expression in the dorsal motor nucleus of the vagus (DMV) neurons projecting to the periphery. Esophageal distension caused 19.7 ± 2.3% of the noradrenergic NTS neurons located 0.60 mm rostral to the calamus scriptorius (CS) to be activated but had little effect on c-Fos in DMV neurons. Intravenous administration of nicotine caused 19.7 ± 4.2% of the noradrenergic NTS neurons 0.90 mm rostral to CS to be activated and, as reported previously, had no effect on c-Fos expression in DMV neurons. To determine whether norepinephrine and nitric oxide were central mediators of esophageal distension-induced decrease in intragastric pressure (balloon recording), N G-nitro-l-arginine methyl ester microinjected into the NTS ( n = 5), but not into the DMV, blocked the Vagovagal Reflex. Conversely, α2-adrenergic blockers microinjected into the DMV ( n = 7), but not into the NTS, blocked the Vagovagal Reflex. These data, in combination with our earlier pharmacological microinjection data with nicotine, indicate that both esophageal distension and nicotine produce nitric oxide in the NTS, which then activates noradrenergic neurons that terminate on and inhibit DMV neurons.
Gerlinda E. Hermann - One of the best experts on this subject based on the ideXlab platform.
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proteinase activated receptors in the nucleus of the solitary tract evidence for glial neural interactions in autonomic control of the stomach
The Journal of Neuroscience, 2009Co-Authors: Gerlinda E. Hermann, Montina J Van Meter, Jennifer Rood, Richard C. RogersAbstract:Bleeding head injury is associated with gastric stasis, a symptom of collapse of autonomic control of the gut described by Cushing around 1932. Recent work suggests that the proteinase thrombin, produced secondary to bleeding, may be the root cause. Results from our in vivo physiological studies show that fourth ventricular injection of PAR1 agonists, as well as thrombin itself, produced significant reductions in gastric transit in the awake rat. We expected that the PAR1 effect to inhibit gastric transit was the result of direct action on Vagovagal Reflex circuitry in the dorsal medulla. Surprisingly, our immunohistochemical studies demonstrated that PAR1 receptors are localized exclusively to the astrocytes and not the neurons in the nucleus of the solitary tract (NST; principal locus integrating visceral afferent input and part of the gastric Vagovagal Reflex control circuitry). Our in vitro calcium imaging studies of hindbrain slices revealed that PAR1 activation initially causes a dramatic increase in astrocytic calcium, followed seconds later by an increase in calcium signal in NST neurons. The neuronal effect, but not the astrocytic effect, of PAR1 activation was eliminated by glutamate receptor antagonism. TTX did not eliminate the effects of PAR1 activation on either glia or neurons. Thus, we propose that glia are the primary CNS sensors for PAR agonists and that the response of these glial cells drives the activity of adjacent (e.g., NST) neurons. These results show, for the first time, that changes in autonomic control can be directly signaled by glial detection of local chemical stimuli.
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Comments on “Hindbrain chemical mediators of Reflex-induced inhibition of gastric tone produced by esophageal distension and intravenous nicotine”
American Journal of Physiology-Regulatory Integrative and Comparative Physiology, 2006Co-Authors: Richard C. Rogers, Gerlinda E. Hermann, R. Alberto TravagliAbstract:The purpose of this study was to activate a Vagovagal Reflex by using esophageal distension and nicotine and test whether hindbrain nitric oxide and norepinephrine are involved in this Reflex function. We used double-labeling immunocytochemical methods to determine whether esophageal distension (and nicotine) activates c-Fos expression in nitrergic and noradrenergic neurons in the nucleus tractus solitarii (NTS). We also studied c-Fos expression in the dorsal motor nucleus of the vagus (DMV) neurons projecting to the periphery. Esophageal distension caused 19.7 ± 2.3% of the noradrenergic NTS neurons located 0.60 mm rostral to the calamus scriptorius (CS) to be activated but had little effect on c-Fos in DMV neurons. Intravenous administration of nicotine caused 19.7 ± 4.2% of the noradrenergic NTS neurons 0.90 mm rostral to CS to be activated and, as reported previously, had no effect on c-Fos expression in DMV neurons. To determine whether norepinephrine and nitric oxide were central mediators of esophageal distension-induced decrease in intragastric pressure (balloon recording), N G-nitro-l-arginine methyl ester microinjected into the NTS ( n = 5), but not into the DMV, blocked the Vagovagal Reflex. Conversely, α2-adrenergic blockers microinjected into the DMV ( n = 7), but not into the NTS, blocked the Vagovagal Reflex. These data, in combination with our earlier pharmacological microinjection data with nicotine, indicate that both esophageal distension and nicotine produce nitric oxide in the NTS, which then activates noradrenergic neurons that terminate on and inhibit DMV neurons.
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Vagovagal Reflex control of digestion: afferent modulation by neural and "endoneurocrine" factors
American Journal of Physiology-Gastrointestinal and Liver Physiology, 1995Co-Authors: Richard C. Rogers, Dana M. Mctigue, Gerlinda E. HermannAbstract:Vagovagal Reflex control circuits in the dorsal vagal complex of the brain stem provide overall coordination of gastric, small intestinal, and pancreatic digestive functions. The neural components forming these Reflex circuits are under substantial descending neural control. By adjusting the excitability of the differing components of the Reflex, significant alterations in digestion control can be produced by the central nervous system. Additionally, the dorsal vagal complex is situated within a circumventricular region without a "blood-brain barrier." As a result, Vagovagal Reflex circuitry is also exposed to humoral influences, which can profoundly alter digestive functions by acting directly on brain stem neurons.
Z Itoh - One of the best experts on this subject based on the ideXlab platform.
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Vagovagal inhibition of motilin-induced phase III contractions by antral acidification in dog stomach.
The American journal of physiology, 1994Co-Authors: O Yamamoto, Y Matsunaga, N Haga, Z ItohAbstract:Gastric acidification at pH 1.0 strongly inhibits the spontaneously occurring and motilin-induced phase III contractions in canine and human stomach. In this study, we examined inhibition by gastric acidification in dogs following gastrojejunostomy, truncal vagotomy, and antrectomy. As a result, gastric acidification with 0.1 N HCl solution at pH 1.0 for 30 min at a rate of 1.0 ml/min significantly inhibited motilin-induced phase III activity to 23.5 +/- 5.9% of the control in the normal intact dogs and to 17.2 +/- 3.4% in the gastrojejunostomized dogs. In the antrectomized dogs, gastric acidification did not significantly inhibit the action of motilin (81.7 +/- 10%), but, in the vagotomized dogs, gastric acidification inhibited the action of motilin to 72.0 +/- 4.9%; the inhibition was much weaker than in the intact and gastrojejunostomized dogs but was significant. The duodenal acidification had no effect at all on the action of motilin (94.6 +/- 12.5%) in the gastrojejunostomized dogs. These findings strongly suggest the existence of a Vagovagal Reflex in the inhibition of motilin-induced phase III contractions by gastric antral acidification, although the involvement of sympathetic regulation cannot be completely ruled out.
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Inhibition of phase III activity by acidifying stomach in vagally denervated and innervated dogs with gastric pouches
Gastroenterology, 1994Co-Authors: O Yamamoto, Y Matsunaga, N Haga, Akiyoshi Mizumoto, Z ItohAbstract:Abstract Background/Aims: Intragastric acidification at pH 1.0 strongly inhibits phase III contractions in the dog, but this mechanism is not well known. We studied the mechanism in conscious dogs. Methods: Vagally denervated and innervated gastric pouch dogs were prepared. Force transducers were chronically implanted on the serosa of the pouch, main stomach, and midduodenum. The pH of the perfusate was monitored. Results: Administration of histamine (40 μg · kg −1 · h −1 intravenously [IV]) and instillation of acidic saline at pH 1.0, but not pH 2.0, into the main stomach strongly inhibited the motilin-induced (0.1 μg/kg IV) phase III activity in the main stomach and the innervated pouch but did not influence contractions in the extrinsically denervated pouch. Famotidine completely reversed the histamine-induced inhibition of phase III in the main stomach and Pavlov pouch. Acidification of the pouch itself or duodenum at pH 1.0 did not affect contractions in the main stomach and pouch of either type. Conclusions: The mechanism of inhibition of motilin-induced phase III activity by acid in the stomach involves the intact Vagovagal Reflex, but sympathetic participation is not completely ruled out. The inhibition of motilininduced phase III activity may originate in the antral mucosa of the stomach.
