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At least 505 records · Page 28Linked to original sources
PubMed1998

Neuropeptide Y inhibits ion secretion in intestinal epithelium by reducing chloride and potassium conductance.

Neuropeptide Y (NPY) is probably the most abundant neuropeptide, with a plethora of central as well as peripheral effects, including its proabsorptive action in the gastro-intestinal tract. The effects of NPY on electrical parameters related to three different pathways stimulating ion secretion were investigated using the human intestinal cell line HT29cl.19A. Transepithelial potential and resistance were measured with the preparation maintained in a horizontal Ussing chamber, allowing simultaneous measurement of the membrane potential and determination of the fractional resistance of the apical cell membrane. It was found that application of NPY, after the adenylyl-cyclase-activating drug forskolin, resulted in complete inhibition of forskolin-induced effects within approximately 20 min. The secretion stimulated by adenosine appeared to be insensitive to NPY. The acetylcholine analogue carbachol stimulates ion secretion by increasing intracellular free calcium concentrations ([Ca2+]i) which activates the basolateral potassium (K+) conductance. NPY caused 50% inhibition of the effect of carbachol. Measurements of [Ca2+]i showed that NPY inhibited the carbachol-induced rise in [Ca2+]i, which correlates with the reduced activation of basolateral K+ channels. From this study we conclude that NPY inhibits cAMP-stimulated as well as Ca2+-stimulated secretion via a reduction in the apical Cl- and basolateral K+ conductance. This double effect makes NPY an effective proabsorptive peptide.

Adenosine↗
PubMed2003

Dietary fructooligosaccharides induce immunoregulation of intestinal IgA secretion by murine Peyer's patch cells.

Probiotic supplements induce immunological responses in the host, and dietary fructooligosaccharides (FOS) stimulate the growth of selected intestinal microflora. In this study we investigated the immunological influences of orally administrated FOS. BALB/c mice were orally administered 0-7.5% FOS for 6 weeks, and the intestinal mucosal immune responses were measured. In the 2.5%-FOS group, fecal IgA was significantly increased. IgA secretion by Peyer's patch (PP) cells was upregulated in a dose-dependent way in response to FOS and CD4+ T cells from PP showed a dose-dependent increase in production of interferon-gamma and interleukin (IL) 10, and a high response in production of IL-5 and IL-6. In contrast, FOS suppressed serum IgG1. Our findings suggest that FOS supplementation changes the intestinal environment of microflora, and leads to upregulation of IgA secretion in CD4+ PP cells in intestinal mucosa, and to suppression of the systemic immune response to type 2 helper T (Th2) dominant.

Adjuvants, Immunologic↗
PubMed1982

Inhibition of gastric acid secretion by intestinal and parenteral administration of a mixture of L-amino acids in the Atlantic cod, Gadus morhua.

The effect on basal gastric acid secretion in the cod of a mixture of L-amino acids (AA) was studied. Acid secretion was measured during a 5 h treatment period when the AA was administered intestinally, i.m. or i.v., and plasma alpha-amino nitrogen following the treatment period. Acid secretion was inhibited, the depression related to the plasma level of AA but unrelated to the administration route. It is suggested that acid secretion is inhibited by absorbed AA acting from the blood side, without involvement of an intestinal mechanism.

Amino Acids↗
PubMed1999

Involvement of serotonin and calcium channels in the intestinal fluid secretion evoked by bile salt and cholera toxin.

1. The enteric nervous system (ENS) is activated when exposing the intestinal mucosa to cholera toxin or certain bile salts. Cholera toxin stimulates ENS, at least in part, by the release of 5-hydroxytryptamine (5-HT) from the enterochromaffin cells. Calcium channel blockers of the L-type markedly attenuate the fluid secretion and the luminal release of 5-HT caused by cholera toxin. 2. The objective of the present study was to elucidate if sodium deoxycholate activated ENS in a similar manner as cholera toxin. Furthermore, the effect of several calcium channel blockers was tested on the fluid secretion caused by cholera toxin or bile salt. 3. Sodium deoxycholate (4 mM) caused a release of 5-HT into the intestinal lumen, which was inhibited by calcium channel blockade. Granisetron, a 5-HT3 receptor blocker, partly inhibited the fluid secretion caused by bile salt. 4. The effects of nifedipine, felodipine, R-felodipine, H186/86 (t-butyl analogue of felodipine) on the fluid secretion caused by cholera toxin or sodium deoxycholate were studied. Both secretory states were markedly attenuated in a dose dependent manner by all calcium channel blockers tested regardless of their effects on arterial pressure. 5. It is concluded that both cholera toxin and bile salt activate ENS, at least in part, via a release of 5-HT from the enterochromaffin cells. The antisecretory effect calcium channel blockers is partly explained by an inhibition of this release of 5-HT.

Animals↗
PubMed1993

Signal transduction pathways mediating mucin secretion from intestinal goblet cells.

Cholinergic stimulation of the HT29-18N2 goblet cell line increased mucin secretion as assessed: (1) with a mucin-specific immunoassay, (2) using whole-mount immunocytochemistry, or (3) by morphometric quantification of intracellular mucous granule stores. Cholinergic stimulation did not, however, result in the apical plasmalemmal membrane cavitation that is characteristic of recent compound exocytotic activity. The response was not dependent on protein kinase C activation since it was not inhibited by the kinase C antagonist H7 or potentiated by the diacylglycerol kinase antagonist R59022. Calcium ionophore A23187 also accelerated mucin secretion by a noncompound exocytotic pathway. Activation of protein kinase C by phorbol 12-myristate 13-acetate, on the other hand, increased mucin secretion by a compound exocytotic pathway. The results provide insight into the signal transduction pathways underlying secretory responses of goblet cells observed in situ.

Adenocarcinoma↗
PubMed2006

Rotavirus infection is not associated with small intestinal fluid secretion in the adult mouse.

In contrast to humans, adult but not infant small animals are resistant to rotavirus diarrhea. The pathophysiological mechanism behind this age-restricted diarrhea is currently unresolved, and this question was investigated by studying the secretory state of the small intestines of adult mice infected with rotavirus. Immunohistochemistry and histological examinations revealed that rotavirus (strain EDIM) infects all parts of the small intestines of adult mice, with significant numbers of infected cells in the ilea at 2 and 4 days postinfection. Furthermore, quantitative PCR revealed that 100-fold more viral RNA was produced in the ilea than in the jejuna or duodena of adult mice. In vitro perfusion experiments of the small intestine did not reveal any significant changes in net fluid secretion among mice infected for 3 days or 4 days or in those that were noninfected (37 +/- 9 microl . h(-1) . cm(-1), 22 +/- 13 microl . h(-1) . cm(-1), and 33 +/- 6 microl . h(-1) . cm(-1), respectively) or in transmucosal potential difference (4.0 +/- 0.3 mV versus 3.9 +/- 0.4 mV), a marker for active chloride secretion, between control and rotavirus-infected mice. In vivo experiments also did not show any differences in potential difference between uninfected and infected small intestines. Furthermore, no significant differences in weight between infected and uninfected small intestines were found, nor were any differences in fecal output observed between infected and control mice. Altogether, these data suggest that rotavirus infection is not sufficient to stimulate chloride and water secretion from the small intestines of adult mice.

Animals↗
PubMed2005

New views on antidiarrheal effect of wood creosote: is wood creosote really a gastrointestinal antiseptic?

Wood creosote, the principal ingredient in Seirogan, has a long history as a known gastrointestinal microbicidal agent. When administered orally, the intraluminal concentration of wood creosote is not sufficiently high to achieve this microbicidal effect. Through further animal tests, we have shown that antimotility and antisecretory actions are the principal antidiarrheal effects of wood creosote. Wood creosote inhibits intestinal secretion induced by enterotoxins by blocking the Cl(-) channel on the intestinal epithelium. Wood creosote also decreases intestinal motility accelerated by mechanical, chemical, or electrical stimulus by the inhibition of the Ca(2+) influx into the smooth muscle cells. In this overview, the antimotility and antisecretory effects of wood creosote are compared with those of loperamide. Wood creosote was observed to inhibit stimulated colonic motility, but not normal jejunal motility. Loperamide inhibits normal jejunal motility, but not stimulated colonic motility. Both wood creosote and loperamide inhibit intestinal secretion accelerated by acetylcholine. Wood creosote was found to have greater antisecretory effects in the colon than loperamide. Based upon these findings, we conclude that the antidiarrheal effects of wood creosote are due to both antisecretory activity in the intestine and antimotility in the colon, but not due to the microbicidal activity as previously thought. Wood creosote was found to have no effects on normal intestinal activity. These conclusions are supported by the results of a recent clinical study comparing wood creosote and loperamide, which concluded that wood creosote was more efficacious in relieving abdominal pain and comparable to loperamide in relieving diarrhea.

Animals↗
PubMed1994

The maintenance of fluid balance during exercise.

Fluid supplementation is necessary for exercise in which fluid losses must be offset by intake to avoid the negative effects of hypohydration on health and performance. Several aspects of gastrointestinal function have been studied to gain information concerning the assimilation of ingested fluids to maintain fluid balance during exercise. Research results with regards to gastric emptying and secretion, intestinal absorption and secretion, and aspects of fluid retention, including urine production and plasma volume changes, can be utilised to formulate an appropriate fluid supplementation regimen. Increasing the volume of ingestate and decreasing the carbohydrate concentration promote gastric emptying of fluids. By maintaining a low osmolality secretion is reduced, thus leading to a greater rate of net fluid absorption. Adding sodium and carbohydrate (up to approximately 7%) increases the net intestinal absorption rate. Increasing carbohydrate concentration above this level begins to have a deleterious effect on intestinal absorption of fluid. Sodium also promotes retention of ingested fluids and leads to an increased plasma volume response during rehydration. The primary goal of supplementation should be considered, fluid vs carbohydrate provision, and the beverage composition altered accordingly. Beverage composition to maximise fluid provision will not maximise carbohydrate availability.

Dehydration↗
PubMed2006

High-viscosity carboxymethylcellulose reduces carbachol-stimulated intestinal chloride secretion in weaned piglets fed a diet based on skimmed milk powder and maltodextrin.

High-viscosity carboxymethylcellulose (CMC) promotes gastrointestinal disorders, tissue alterations and bacterial overgrowth in pigs. The impact of CMC on intestinal absorptive and secretory physiology is not known. We hypothesised that CMC consumption alters intestinal Na-dependent glucose absorption and stimulates electrogenic chloride secretion. For testing this hypothesis, twenty-four piglets were weaned at 21 d of age and pair-fed for 13 d a starter diet based on skimmed milk powder and maltodextrin containing cellulose (control) or CMC. Body weight and faecal total aerobe and coliform counts were measured kinetically. At slaughter, digesta were weighed and characterised for viscosity and pH. Gastrointestinal tissues were weighed and sampled for physiology in Ussing chambers, morphometry and enzymology. Glucose absorption tended to be higher (P = 0.08) and carbachol-stimulated chloride secretion was lower (P = 0.01) with CMC in the small intestine, without changes in the colon. Aerobes were transiently higher at day 7 (P < 0.05) but coliform counts remained unchanged (P = 0.78) and beta-haemolitic Escherichia coli were virtually absent. Stomach and small-intestinal segments were heavier, and viscosity higher with CMC (0.001 < P < 0.05). The pH in the stomach was higher, and in the caecum and proximal colon lower with CMC (0.001 < P < 0.05). Jejunal villus area was slightly reduced with CMC (P < 0.05) without effects on enzyme activities (P > 0.10). In conclusion, CMC supplementation had pro-absorptive effects on the small intestine, possibly due to the absence of pathogenic E. coli in the present study.

Animals↗
PubMed1984

Antithrombin, antitrypsin and antichymotrypsin activities of the salivary gland secretion and intestinal chyme of medicinal leeches. Antichymotrypsin activity of partially purified preparations of hirudin and pseudohirudin.

High antithrombin activity was maintained in the salivary gland secretion of starved medicinal leeches (Hirudo medicinalis) despite harvesting of the secretion twice in a month. However, after third or fourth harvesting every month antithrombin activity was no longer detectable. Moreover, in salivary gland secretion high antitrypsin activity was found but no antichymotrypsin activity. On the other hand, intestinal chyme of starved leeches exhibited high antichymotrypsin activity. Low antithrombin and antitrypsin activities were due to contamination by salivary gland secretion. There was a correlation between antichymotrypsin and antithrombin activities of hirudin preparations purified from bdellins and fractionated by isoelectric focusing. Pseudohirudin preparations exhibited neither antithrombin nor antichymotrypsin activities.

Animals↗
PubMed1993

Differences in cytokine secretion by intestinal mononuclear cells, peripheral blood monocytes and alveolar macrophages from HIV-infected patients.

Mononuclear cells of the lamina propria (LpMNC), isolated from endoscopically taken biopsies of the large bowel from AIDS patients, were analysed for their ability to secrete tumour necrosis factor-alpha (TNF-alpha), IL-1 beta and IL-6. Stimulation of LpMNC from normal controls with pokeweed mitogen (PWM) led to a time- and dose-dependent enhancement of TNF-alpha, IL-1 beta and IL-6 secretion. In contrast, PWM stimulation of LpMNC from AIDS patients resulted in only a small increase in TNF-alpha release. Constitutive secretion of IL-1 beta and IL-6 in these patients was already increased to the concentration range of stimulated cells from normal controls and could not be further increased, probably due to maximal in vivo stimulation. Secretion of TNF-alpha, IL-1 beta and IL-6 by peripheral blood monocytes (PBM) and alveolar macrophages from AIDS patients was elevated with or without stimulation compared with normal controls. Obviously, the regulation of TNF-alpha secretion is dependent on the microenvironment. Since it is known that interferon-gamma (IFN-gamma) may induce the production of TNF-alpha, the secretion of this cytokine was examined. Release of IFN-gamma was constitutively and under stimulation lowered in LpMNC from AIDS patients compared with normal controls. Addition of IFN-gamma to LpMNC did not result in enhanced TNF-alpha secretion. Our data indicate a defective function of intestinal mononuclear cells in AIDS patients as shown by the diminished TNF-alpha secretion.

HIV Infections↗
PubMed1997

Role of platelet-activating factor in Chinese hamster ovary cell responses to cholera toxin.

Cholera toxin (CT)-induced intestinal secretion and Chinese hamster ovary cell (CHO) elongation involves cyclic adenosine monophosphate and protein synthesis-dependent prostaglandin formation. We previously reported inhibition of CT-induced intestinal secretion and CHO elongation by platelet-activating factor (PAF) receptor antagonists and secretion of PAF by human intestinal epithelial cells exposed to CT. Herein, we show that PAF is involved after cAMP and that PAF, like CT, mediates prostaglandin E2 synthesis in CHO cells. CT-induced CHO elongation was blocked by specific PAF receptor antagonists, BN52021 and SR27417. SR27417 blocked dibutyryl cAMP-induced CHO elongation, but did not alter CHO elongation caused by PGE2. Neither CT-stimulated cAMP accumulation nor PGE2 production was inhibited by SR27417. Both PGE2 and PAF caused significant CHO elongation, but the latter did not stimulate significant cAMP production. In addition, PAF, like CT and dibutyryl cAMP, stimulated significant PGE2 production. Finally, the protein synthesis inhibitor cycloheximide, which completely blocks the effect of CT on prostaglandin synthesis, also blocked that of PAF, suggesting that PAF also mediates protein synthesis-dependent prostaglandin formation. We conclude that PAF is involved in CHO cytoskeletal responses to CT after the accumulation of cAMP and, like CT, PAF stimulates protein synthesis-dependent prostaglandin accumulation.

Alprostadil↗
PubMed1998

Vasoactive intestinal peptide secretion by turkey hypothalamic explants.

The objective of this study was to culture turkey hypothalami and examine vasoactive intestinal peptide (VIP) release during the turkey reproductive cycle. The release of VIP was studied employing a computer-guided perifusion system. Hypothalami were perifused with Krebs-Ringer bicarbonate medium for 10 or 15 h at a flow rate of 40 microliter/min, and perifusate was collected at 5-min intervals. Basal VIP secretion increased (p < 0.05) over time, and no differences in release rate were noted between reproductive stages. Basal VIP release during perifusion was episodic throughout each experimental period. Perifusion with dopamine (DA; 10 and 100 nmol/min) in incubating hens stimulated VIP release in a dose-dependent manner. There were no significant differences (p > 0.05) in VIP release in response to DA stimulation between hypothalamic fragments obtained from nonphotostimulated and incubating birds. The data suggest that 1) a VIP pulse generator appears to be located within the turkey hypothalamus, on the basis of the observed pulsatile release of VIP; 2) hypothalamic secretion of VIP is augmented by removal of inhibitory factors residing outside of the hypothalamus, or by the loss of negative feedback mechanisms that inhibit VIP release; and 3) mechanisms responsible for altering VIP release during different reproductive conditions may lie external to the hypothalamus.

Animals↗
PubMed1981

Intestinal bicarbonate secretion in Amphiuma measured by pH stat in vitro: relationship with metabolism and transport of sodium and chloride ions.

1. Isolated Amphiuma small intestine exposed on both surfaces to buffered or unbuffered media generated gradients of pH under short-circuited conditions consistent with secretion of HCO3(-). 2. When unbuffered mucosal medium was maintained at pH 7.4 by addition of acid, alkalinization of the mucosal medium occurred at a rate of 1-2 microequiv/hr cm2 under short-circuit conditions (Isc) and was reduced by anoxia, acetazolamide or removal of CO2. 3. The rate of HCO3(-) secretion (JHCO3(-)) was reduced at a mucosal pH above or below 7.4 and was proportional to serosal HCO3(-). 4. JHCO3(-) was reduced in Na+-free (choline) and Cl-free (SO4(2-) media and after exposure to the stilbene SITS. 5. The difference JHCO3(-)--Isc was consistent with net Cl- absorption. 6. The tissue resistance (Rt) was elevated upon exposure to serosal HCO3(-) and lowered by mucosal HCO3(-). 7. The intestinal mucosa exhibited carbonic anhydrase activity that was sensitive to ethoxazolamide. 8. It is concluded that HCO3(-) secretion is active, influenced by intracellular carbonic anhydrase activity and coupled to Cl- and possibly Na+ absorption.

Animals↗
PubMed1999

The role of the pancreas in intestinal zinc secretion in metallothionein-null mice.

The distribution and excretion of endogenous Zn, including the role of the pancreas, were examined in fasted MT+/+ and MT-/- mice. At 3 and 6 h after receiving 65Zn tracer by subcutaneous injection, 65Zn levels were compared in tissues of MT+/+ and MT-/- mice. 65Zn levels were significantly higher in the liver and pancreas of the MT+/+ mice, whereas in the MT-/- mice, 65Zn levels were significantly higher in muscle, skin, and most of the gastrointestinal tract other than the stomach and upper small intestine. In MT-/- mice, 3% of the injected 65Zn was recovered in the luminal contents of the small intestine over 3-6 h, compared with <1.5% in the MT+/+ mice. A loading dose of Zn (150 microg, s.c.) sufficient to raise the plasma Zn concentration by fourfold to fivefold in both MT+/+ and MT-/- mice resulted in similar increases in pancreatic Zn levels in each genotype, although more Zn appeared in the lower small intestine of MT-/- mice. Pancreatectomy decreased the level of 65Zn in the small intestine of MT-/- but not MT+/+ mice. Longer-term studies over 4 days demonstrated few differences in tissue 65Zn between MT+/+ and MT-/- mice, with the exception of the pancreas, where 65Zn retention after fasting in MT-/- mice was half that of MT+/+ mice. MT-/- mice also had significantly lower Zn concentrations in the pancreas. Fecal excretion of 65Zn in MT-/- mice was greater than that of MT+/+ mice in the first 24 h (24.7 vs. 18.2% of injected dose; p < 0.05). Besides metallothionein (MT), there were no significant differences in the molecular weight distribution of Zn binding ligands in the lumen of the small intestine between MT+/+ and MT-/- mice. Mice lacking MT I and II lose more endogenous Zn into the gut because of a relative failure of the pancreas to retain Zn. However, increased Zn secretion via the small intestinal mucosa may also contribute to intestinal Zn loss in MT-/- mice.

Animals↗
PubMed1990

Immune-related intestinal chloride secretion. II. Effect of adenosine on T84 cell line.

The inflammatory mediator adenosine caused sustained Cl- secretion across monolayers of T84 cells. The effect was promptly reversed by the adenosine receptor antagonist 8-phenyltheophylline and appeared to be mediated through an adenosine A2-receptor [rank order of potency: 5'-(N-ethyl)-carboxamido-adenosine (NECA) greater than adenosine greater than (-)-N6-(phenylisopropyl)adenosine (PIA) greater than or equal to (+)-PIA]. High doses of adenosine and its analogues increased cellular adenosine 3',5'-cyclic monophosphate (cAMP) but not guanosine 3',5'-cyclic monophosphate (cGMP) or free cytosolic Ca2+. However, lower concentrations of adenosine had maximal effects on Cl- secretion with little or no effect on cAMP. In other respects, Cl- secretion resembled that induced by cAMP-mediated secretagogues such as vasoactive intestinal peptide (VIP). Addition of both low and high doses of NECA activated basolateral K+ and apical Cl- channels, exhibited synergism with Ca2(+)-mediated secretagogues, did not produce additive effects with VIP or Escherichia coli heat-stable enterotoxin, and was associated with cAMP-dependent protein kinase-mediated protein phosphorylation. The results suggest that either adenosine mobilizes an intracellular pool of cAMP that is extremely efficiently coupled to the cAMP-dependent protein kinase and is thereafter rapidly destroyed or that second messenger(s) other than cAMP, cGMP, or Ca2+ are able to activate Cl- secretion in the T84 cell line. In the latter case, such messenger(s), as yet unidentified, might represent a final common pathway for cyclic nucleotide-activated Cl- secretion.

2-Chloroadenosine↗
PubMed1993

Comparative effects of nicotinic acid and nicotinamide on cholera toxin-induced secretion in rabbit ileum.

Nicotinic acid reduces the cholera-toxin induced fluid secretion in experimental animals but its toxicity at high doses prevent its therapeutic use in patients suffering from cholera. This study aimed to determine whether nicotinamide, the non toxic amide derivative of nicotinic acid, is as effective as nicotinic acid in inhibiting cholera toxin induced intestinal secretion in vivo. Four intestinal loops, with their blood supply intact, were isolated in 30 rabbits and injected with either (i) 30 mM mannitol, (ii) 30 mM mannitol + 10 micrograms cholera toxin, (iii) 30 mM glucose, or (iv) 30 mM glucose + 10 micrograms cholera toxin. These rabbits were then randomly assigned to three groups receiving intraluminally either 100 mg/kg of nicotinic acid, 100 mg/kg of nicotinamide, or 10 ml/kg of Ringer solution. Measurement of intestinal fluid accumulation showed that nicotinic acid, but not nicotinamide, significantly reduced cholera toxin induced intestinal secretion.

Animals↗
PubMed1990

Pathophysiology of acute diarrhea.

Diarrhea, a major health problem worldwide, is both a sign and a symptom. As a symptom, diarrhea has been described as an increase in stool frequency, an increase in stool volume, and/or a decrease in stool consistency. As a sign, diarrhea is characterized by an increase in stool water excretion to greater than 150 to 200 ml every 24 hours. Four mechanisms that may be responsible for the alterations in fluid and electrolyte movement associated with diarrhea are increased luminal osmolality, decreased fluid absorption, increased intestinal secretion, and altered intestinal motility. Specific pathogenic mechanisms for acute infectious diarrhea include tissue invasion, enterotoxin production, and adhesion of infectious agents to epithelial cells. Antidiarrheal agents remove secretagogues from the intestinal tract, stimulate fluid absorption, and inhibit electrolyte movement.

Acute Disease↗