Action of Serotonin on the Gastrointestinal Tract

Ormsbee, Herbert S.; Fondacaro, Joseph D.

doi:10.3181/00379727-178-42016

Cited by 83 publications

(35 citation statements)

References 13 publications

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“…Apart from CCK, several other gastrointestinal hormones are released during digestion, including somatostatin, leptin, gastrin, secretin, peptide YY, enteroglucagon, neurotensin (13,43), and 5-HT (32). Although the ability of CCK to augment gastrointestinal blood flow has been demonstrated (4,10,15,39), other gastrointestinal hormones have been implicated in postprandial gastrointestinal hyperemia (4,36).…”

Section: Discussionmentioning

confidence: 99%

An enteric signal regulates putative gastrointestinal presympathetic vasomotor neurons in rats

Sartor¹,

Shulkes²,

Verberne³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Sartor, Daniela M., Arthur Shulkes, and Anthony J. M. Verberne. An enteric signal regulates putative gastrointestinal presympathetic vasomotor neurons in rats. Am J Physiol Regul Integr Comp Physiol 290: R625-R633, 2006. First published October 20, 2005 doi:10.1152/ajpregu.00639.2005.-Ingestion of a meal results in gastrointestinal (GI) hyperemia and is associated with systemic and paracrine release of a number of peptide hormones, including cholecystokinin (CCK) and 5-hydroxytryptamine (5-HT). Systemic administration of CCK octapeptide inhibits a subset of presympathetic neurons of the rostroventrolateral medulla (RVLM) that may be responsible for driving the sympathetic vasomotor tone to the GI viscera. The aim of this study was to determine whether endogenous release of CCK and/or 5-HT also inhibits CCK-sensitive RVLM neurons. The effects of intraduodenal administration of the secretagogues sodium oleate (SO) and soybean trypsin inhibitor (SBTI) on circulating levels of CCK and 5-HT were examined. In separate experiments, the discharge rates of barosensitive, medullospinal, CCK-sensitive RVLM presympathetic vasomotor neurons were recorded after rapid intraduodenal infusion of SO-SBTI or water. Alternatively, animals were pretreated with the CCK 1 receptor antagonists devazepide and lorglumide or the 5-HT 3 antagonist MDL-72222 before SO-SBTI administration. Secretagogue infusion significantly increased the level of circulating CCK, but not 5-HT. SO-SBTI significantly decreased (58%) the neuronal firing rate of CCKsensitive RVLM neurons compared with water (5%). CCK 1 receptor antagonists did not reverse SO-SBTI-induced neuronal inhibition (58%), whereas the 5-HT 3 antagonist significantly attenuated the effect (22%). This study demonstrates a functional relation between a subset of RVLM presympathetic vasomotor neurons and meal-related signals arising from the GI tract. It is likely that endogenously released 5-HT acts in a paracrine fashion on GI 5-HT 3 receptors to initiate reflex inhibition of these neurons, resulting in GI vasodilatation by withdrawal of sympathetic tone. rostroventrolateral medulla; cholecystokinin; devazepide; MDL-72222; 5-hydroxytryptamine GASTROINTESTINAL HYPEREMIA is a physiological consequence of food consumption. Gastrointestinal hormones such as cholecystokinin (CCK) have been implicated in gastrointestinal vasodilatation associated with postprandial increase in splanchnic blood flow. The involvement of the sympathetic vasomotor system in this response is poorly understood. We recently suggested that food-related signals may produce gastrointestinal vasodilatation via a reflex withdrawal of sympathetic vasomotor outflow (39,45). In healthy individuals, the sympathetic nervous system compensates for postprandial splanchnic blood pooling by activating sympathetic vasoconstrictor drive to skeletal muscle resistance vessels in response to baroreceptor unloading. In patients with cardiovascular disease associated with diabetic neuropathy or autonomic dysfunction, poor baroreflex comp...

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Section: Discussionmentioning

confidence: 99%

An enteric signal regulates putative gastrointestinal presympathetic vasomotor neurons in rats

Sartor¹,

Shulkes²,

Verberne³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Only a portion of the growth improvement could be accounted for by feed intake differences and this has also been observed by Cortamira et al (1991). The putative neurotransmitter metabolite of trp, serotonin (5-hydroxytryptamine), is produced and is active in the digestive tract (Orsmbee and Fondacaro, 1985), the circulatory system (Folk and Long, 1988) and nervous tissues (Schaechter and Wurtman, 1990). Oral trp administration has been shown to increase serotonin concentrations in the plasma and brain (Leathwood and Fernstrom, 1990;Adeola and Ball, 1992;Henry et al, 1992), and to accelerate gastric emptying rate (Ponter et al, 1994) and digesta passage rate.…”

Section: Discussionmentioning

confidence: 99%

Bioavailability of threonine and tryptophan in peanut meal for starter pigs using slope-ratio assay

Adeola

2009

Animal

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The objective of the two studies was to determine the bioavailability of threonine (thr) and tryptophan (trp) in peanut meal, relative to L-thr and L-trp, for starter pigs using the slope-ratio bioassay. Basal diets (BDs) contained surfeit amounts of all amino acids for 10 to 20 kg pigs, except for thr (Experiment 1) or trp (Experiment 2). In the first study, four reference diets were formulated by supplementing the BD with 0, 0.4, 0.8 or 1.2 g of L-thr/kg at the expense of cornstarch; two test diets were formulated by replacing cornstarch in the BD with peanut meal at 32 or 64 g/kg of diet to supply 0.4 or 0.8 g thr/kg, respectively. Four reference diets consisting of the BD supplemented with 0, 0.15, 0.3 or 0.45 g of L-trp/kg at the expense of cornstarch and two test diets in which cornstarch in the BD was replaced with peanut meal at 30 or 60 g/kg of diet to supply 0.14 or 0.28 g trp/kg, respectively were used in the second study. Body weight gain responded in a linear way to supplemental L-thr or thr from peanut meal ( P , 0.001). There was a linear response ( P , 0.001) to thr supplementation from L-thr or peanut meal in gain-to-feed ratio. The addition of trp to the BD linearly increased ( P , 0.05) body weight gain, feed intake and gainto-feed ratio regardless of the trp source. Common-intercept, multiple linear regression in slope-ratio methodology using weight gain or gain-to-feed ratio as dependent variables and supplemental thr intake as independent variable gave relative bioavailability estimates of 71.9% or 75.7%, respectively. Corresponding values for trp were 92% and 75.7%. The fiducial limits for none of the relative bioavailability estimates included 100%. The data from these studies suggest that the bioavailabilities of thr and trp in peanut meal are less than those of L-thr and L-trp, and that the bioavailabilities of thr and trp in peanut meal are 72% to 76% and 76% to 92%, respectively.

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“…In mice, in vivo, buspirone relaxed the fundus, whereas sumatriptan contracted it (29). There are two sources for 5-HT in the gut: release from enterochromaffin (EC) cells in the mucosa and from myenteric interneurons (21). Additionally, in some species, including mice, mast cells contain 5-HT (4).…”

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confidence: 99%

Serotonergic modulation of murine fundic tone

Lü

Camilleri²,

Locke³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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Fundic tone is maintained through a balance of excitatory and inhibitory input to fundic smooth muscle. The aim of this study was to determine the role of serotonin (5-HT) and 5-HT receptors in modulating murine fundic tone. Muscle strips were prepared from the murine fundus. Intracellular recordings were made from circular smooth muscle cells, and the effects of 5-HT on tone and excitatory and inhibitory junction potentials evoked by electrical field stimulation (EFS) were determined. 5-HT induced a concentration-dependent contraction and smooth muscle depolarization that was tetrodotoxin resistant. The 5-HT 1B/D receptor antagonists GR-127935 and BRL-155172 significantly inhibited 5-HT-induced contractions. The 5-HT 1B/D agonist sumatriptan contracted murine fundic muscle. The 5-HT 1A receptor agonist buspirone relaxed fundic smooth muscle, and the relaxation was inhibited by WAY-100135 but not by N -nitro-L-arginine or tetrodotoxin. 5-HT enhanced both the excitatory and inhibitory responses to EFS. The 5-HT 3 receptor antagonist MDL-72222 partly inhibited both the excitatory and inhibitory response elicited by EFS, whereas the 5-HT 4 receptor antagonist GR-113808 partly inhibited the EFS-evoked inhibitory response. The 5-HT reuptake inhibitor fluoxetine contracted smooth muscle strips, a contraction that was partially inhibited by GR-127935 and abolished by tetrodotoxin. In conclusion, the data suggest that 5-HT modulates murine fundic contractile activity through several different receptor subtypes. Sustained release of 5-HT maintains fundic tone through postjunctional 5-HT 1B/D receptors. 5-HT 3 receptors modulate excitatory neural input to murine fundic smooth muscle, and both 5-HT 3 and 5-HT4 receptors modulate inhibitory neural input to murine fundic smooth muscle.receptors; smooth muscle; enteric nerves; fundic accommodation; serotonin THE STOMACH WALL relaxes to accommodate the entry of content. Relaxation allows the accommodation of a large volume of content without a marked increase in intragastric pressure (7,15). Although there is evidence that the antrum accommodates after a meal, gastric accommodation occurs predominantly in the proximal stomach, especially in the fundus. The fundic integrated relaxatory response to a meal is known as fundic accommodation. The accommodation response is mediated through an extrinsic vagovagal reflex pathway and a nonvagal intrinsic reflex pathway. Both pathways act on intrinsic noncholinergic, nonadrenergic (NANC) neurons in the fundus and other parts of the stomach wall to relax smooth muscle cells (1,3,26,28). In the fasted state, well-established mediators of gastric fundic tone are vagally mediated cholinergic input (2, 29) and NANC inhibitory input (11, 12). The regulation of fundic tone is also mediated through serotonin (5-HT). In humans, sumatriptan, a 5-HT 1B/D agonist, relaxes the fundus (24, 25). In mice, in vivo, buspirone relaxed the fundus, whereas sumatriptan contracted it (29). There are two sources for 5-HT in the gut: release from enterochromaffi...

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Action of Serotonin on the Gastrointestinal Tract

Cited by 83 publications

References 13 publications

An enteric signal regulates putative gastrointestinal presympathetic vasomotor neurons in rats

An enteric signal regulates putative gastrointestinal presympathetic vasomotor neurons in rats

Bioavailability of threonine and tryptophan in peanut meal for starter pigs using slope-ratio assay

Serotonergic modulation of murine fundic tone

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