NO mediates gastric relaxation after brief vagal stimulation in anesthetized dogs

Meulemans, A.L.; Eelen, Jan; Schuurkes, J. A. J.

doi:10.1152/ajpgi.1995.269.2.g255

Cited by 30 publications

(30 citation statements)

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“…72). Much of the vagal NANC inhibitory effect on the stomach is mediated by the release of nitric oxide onto gastric smooth muscle (1,10,24,37,41,44,45,68). Perfusion with CCK-8s induces an excitation in most neurons, including identified gastrointestinal-projecting DMV neurons (4,7,13,23,38,47,48,65,66,75,79).…”

Section: Discussionmentioning

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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Section: Discussionmentioning

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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“…Gastric relaxation is mediated through a vagovagally driven nonadrenergic noncholinergic (NANC) mechanism (2). Both in vivo and in vitro studies suggest that the principal candidate neurotransmitters released by NANC neurons during gastric accommodation are nitric oxide and vasoactive intestinal polypeptide (4,6,7,13,22,26,41). Depending on the species studied, both inhibitory neurotransmitters can act concurrently in mediating NANC relaxations of the fundus (6,22,39,41), or nitric oxide can be the only mediator of the NANC relaxation (13,26,27).…”

Section: Discussionmentioning

confidence: 99%

“…Both in vivo and in vitro studies suggest that the principal candidate neurotransmitters released by NANC neurons during gastric accommodation are nitric oxide and vasoactive intestinal polypeptide (4,6,7,13,22,26,41). Depending on the species studied, both inhibitory neurotransmitters can act concurrently in mediating NANC relaxations of the fundus (6,22,39,41), or nitric oxide can be the only mediator of the NANC relaxation (13,26,27). Enhancement of meal-induced gastric relaxation by sildenafil suggests involvement of nitric oxide in the gastric accommodation reflex in humans, and this observation is in agreement with our previous observation that nitric oxide synthase inhibition significantly inhibits gastric accommodation in humans (37).…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies, both in animals and in humans, have established that this accommodation reflex involves the activation of inhibitory nitrergic neurons in the gastric wall (3,4,13,16,21,26,37). Recent studies have established that impaired accommodation to a meal is a major pathophysiological mechanism in functional dyspepsia (14,31,42), and restoration of accommodation is considered a valid therapeutic target (12,38).…”

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confidence: 99%

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Influence of sildenafil on gastric sensorimotor function in humans

Sarnelli¹,

Sifrim²,

Janssens³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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After a meal, the proximal stomach relaxes probably through the activation of nitrergic neurons in the gastric wall. Nitric oxide-induced smooth muscle relaxation involves activation of soluble guanylate cyclase, with cGMP production, which is then degradated by phosphodiesterase-5 (PDE-5). The aim of this study was to investigate the effect of sildenafil, a selective PDE-5 inhibitor, on fasting and postprandial proximal gastric volume and on gastric emptying rates in humans. A gastric barostat was used to study gastric compliance and perception to isobaric distension in healthy subjects before and after placebo (n ϭ 13) or sildenafil, 50 mg (n ϭ 15). In 10 healthy subjects, two gastric barostat studies were performed in randomized order to study the effect of placebo or sildenafil on postprandial gastric relaxation. Similarly, solid and liquid gastric emptying rates were studied in 12 healthy subjects. Sildenafil significantly increased fasting intragastric volume (141 Ϯ 15 vs. 163 Ϯ 15 ml, P Ͻ 0.05) and volumes of first perception. Sildenafil induced a higher and prolonged gastric relaxation either at 30 min (357 Ϯ 38 vs. 253 Ϯ 42 ml, P Ͻ 0.05) or 60 min (348 Ϯ 49 vs. 247 Ϯ 38 ml, P Ͻ 0.05) after the meal. Sildenafil did not alter solid half-emptying time but significantly delayed liquid emptying (43 Ϯ 4 vs. 56 Ϯ 4 min, P Ͻ 0.01). In conclusion, sildenafil significantly increases postprandial gastric volume and slows liquid emptying rate, confirming that meal-induced accommodation in humans involves the activation of a nitrergic pathway. The effect of sildenafil on gastric fundus suggests a therapeutic potential for phosphodiesterase inhibitors in patients with impaired gastric accommodation. nitric oxide; gastric accommodation; gastric sensitivity; gastric emptying

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“…It has been shown to mediate lower oesophageal sphincter relaxation in animals [29, 30]and man [31]. Vagally induced gastric relaxation occurs via a nitric oxide-dependent mechanism [32, 33]. Duodenal distension also causes reflex gastric relaxation via nitric oxide [34].…”

Section: Discussionmentioning

confidence: 99%

Gastric Compliance, Sensation, and the Relaxation Response to a Nitric Oxide Donor in Health and Reflux Oesophagitis

Newton

Kamm²,

Burnham³

et al. 1999

Digestion

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Background/Aims: The gastric fundus affects afferent control of lower oesophageal sphincter function. Nitric oxide is an important relaxant of the fundus. We postulated that gastric distensibility, compliance and nitric oxide sensitivity may be altered in patients with gastro-oesophageal reflux disease (GERD). Methods: 9 patients with erosive oesophagitis (6 males; median age 55 years) and 16 healthy controls (9 males; median age 36 years) were studied fasting with a gastric barostat. Minimal distending pressure (MDP) and gastric compliance (Δv/Δp) were determined by increasing intrabag pressure in 2-mm Hg increments. The pressures required to produce initial sensation and maximum tolerated sensation were recorded. With the intrabag pressure set at MDP +2 mm Hg, 500 μg sublingual glyceryl trinitrate was administered and the percentage change in intrabag volume from initial volume recorded. Results: The MDP was significantly greater in patients than controls (7.5 vs. 6.7 mm Hg median; p = 0.02). Gastric compliance was similar in both groups (57.8 vs. 67.2 ml/mm Hg; p = 0.4). There was no difference between groups in the pressure at first intragastric sensation (11.2 vs. 10.3 mm Hg above MDP; p = 0.5) or in the maximal tolerated pressure (15.8 vs. 14.3 mm Hg above MDP; p = 0.2). The proportional change in gastric volume from baseline in response to glyceryl trinitrate was smaller in patients than controls (66 (3–200) vs. 120 (26–1,053)%; p = 0.02). Conclusions: Gastric MDP may be altered in GERD, but gastric compliance and sensitivity to distension are normal. Major gastric relaxation occurs in response to a nitric oxide donor, but this appears to be diminished in patients with GERD. Upper gut nitrinergic mechanisms may be altered in oesophageal reflux disease.

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NO mediates gastric relaxation after brief vagal stimulation in anesthetized dogs

Cited by 30 publications

References 0 publications

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

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

Influence of sildenafil on gastric sensorimotor function in humans

Gastric Compliance, Sensation, and the Relaxation Response to a Nitric Oxide Donor in Health and Reflux Oesophagitis

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