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PubMed1994

The adenosine agonist NECA inhibits intestinal secretion and peristalsis.

This study aimed to determine whether the antidiarrhoeal effect of the mixed A1/A2 adenosine agonist NECA (5'-N-ethylcarboxamido adenosine) is due to inhibition of intestinal fluid transport or to contractility. Intestinal secretion was stimulated in anaesthetized rats by intra-arterial infusions of PGE2 (4 micrograms min-1) or vasoactive intestinal peptide (0.8 micrograms min-1). NECA reversed PGE2-induced secretion in the jejunum (ED50 16 micrograms kg-1) and ileum (ED50 21 micrograms kg-1, i.v.) and inhibited VIP-induced secretion in the jejunum (ED50 21.5 micrograms kg-1). NECA inhibited twitch responses (0.1 Hz, 1 ms, IC50 11.2 nM) but not tetanic contractions at 10 Hz of the transmurally stimulated guinea-pig ileum. Likewise, NECA (10 microM) did not inhibit frequency-related contractions over the range of 2.5 to 40 Hz of rat jejunum or ileum. However, NECA was shown to be a potent inhibitor (30 nM) of the peristaltic reflex in the rat ileum. The results indicate that adenosine receptors are involved in modulating peristalsis as well as the secretory activity of the mucosa in the rat small intestine.

Adenosine↗
PubMed1973

Studies on the quantitation of immunoglobulin in human intestinal secretions.

There is increasing evidence for the importance of the secretory immune system in the gut. In studies of local antibody production it is important to have satisfactory methods for measuring immunoglobulin concentrations and to be aware of the errors which may occur. Studies on immunoglobulin measurement in intestinal secretion by the radial immunodiffusion method are reported, showing the effects of proteolytic digestion, IgA molecular size, and sampling and storage conditions. Because of the presence of monomeric IgA in addition to secretory IgA, there is no satisfactory standard for IgA in gastrointestinal secretions, and only semi-quantitative results can be given. With radial immunodiffusion, IgG and IgM when subjected to tryptic digestion, and IgA when subjected to peptic digestion, may be overestimated because of the presence of fragments of immunoglobulins. In addition, pepsin rapidly destroys IgM and IgG. Both IgM and IgG are unstable in storage. The findings suggest that immunoglobulin concentration measurements in small intestinal aspirates should be interpreted with caution. These problems are also relevant to the detection of specific antibodies in gastrointestinal secretions.

Chromatography, Gel↗
PubMed1981

Inhibition of intestinal secretion in rats by colchicine and vinblastine.

The role of microtubules in small intestinal electrolyte secretion was investigated in rats by testing the effects of colchicine and vinblastine, both of which inhibit microtubule assembly. In the intact rat, intraperitoneal injection of colchicine (5 mg/kg) inhibited cholera toxin and prostaglandin-stimulated secretion without inhibiting their effects on adenylate cyclase or cAMP concentration. Pretreatment with colchicine had no effect on fluid transport in the absence of secretory stimuli. When added to rat ileum in vitro, colchicine reduced by 60% the short-circuit current (Isc) response to dibutyryl cAMP added 4 h later, whereas its structural isomer, lumicolchicine, which does not inhibit microtubule assembly, was ineffective. Vinblastine reduced by 55% the Isc response to dibutyryl cAMP and theophylline added 2 h later. Two hour pretreatment with vinblastine also reduced by 40% the Isc response to the cholinergic agonist, carbamylcholine, a Ca-dependent secretory stimulus which does not increase cAMP concentration. In contrast to their antisecretory actions, neither colchicine nor vinblastine inhibited glucose-stimulated active Na absorption. These results suggest a role for microtubules in active electrolyte secretion in the small intestine.

Adenylyl Cyclases↗
PubMed1977

Immunoglobulin in intestinal secretions.

The objective of the present investigation is the study and interpretation of the role played by the immunoglobulins, especially IgA, during acute diarrhea in children. IgA, IGG and IgM values in serum and IgA in intestinal secretions were studied in a group of children (between 3 months and 5 years of age) during diarrhea, convalescence and in normals. The method of simple radial immunodiffusion according to Mancini was employed. IgA is the immunoglobulin which suffers the greastest alteration in acute diarrhea. The precipitation halos (the average values), were lower during the diarrhea than in convalescence and in normals.

Child, Preschool↗
PubMed1996

Role of prostaglandins and enteric nerves in Escherichia coli heat-stable enterotoxin (STa)-induced intestinal secretion in pigs.

OBJECTIVE: To examine the role of prostaglandins and enteric nerves in mediating intestinal secretion induced by enterotoxigenic Escherichia coli heat-stable enterotoxin (STa) in pig jejunum and distal portion of the colon. ANIMALS: Two- to 3-week-old suckling crossbred pigs were studied. DESIGN: Changes in ion transport in response to mucosal addition of E coli STa to jejunal and colonic tissues were studied in the presence and absence of inhibitors. PROCEDURE: Flat sheets of muscle-stripped proximal portions of the jejunum and distal portions of the colon were mounted in Ussing chambers equipped to measure changes in short-circuit current (Isc), a measure of active ion transport. Tissues were exposed to 200 ng of STa/ml administered to mucosal solutions, and subsequent changes in Isc were recorded. RESULTS: In control tissues, changes in Isc induced by STa in the distal colon were significantly greater (21.4 +/- 4 muA/cm2) than those observed in the jejunum (14.0 +/- 2 muA/cm2). When either segment was exposed to the neurotoxin, tetrodotoxin, or to the nitric oxide synthase inhibitor, N(G)-nitro-L-arginine-methyl ester, Isc responses to STa were unchanged, suggesting no involvement of submucosal nerves in mediating STa-induced secretion. When tissues from the distal portion of the colon and jejunum were pretreated with piroxicam, a prostaglandin synthesis inhibitor, the STa-induced Isc response was significantly reduced by 52 and 57%, respectively. CONCLUSIONS: These results indicate that the pig jejunum and distal portion of the colon are sensitive to the secretory actions of enterotoxigenic E coli STa, and that the responses are mediated, in part, by release of prostaglandins.

Animals↗
PubMed2003

Role of mast cells and pro-inflammatory mediators on the intestinal secretion induced by cholera toxin.

Recent data suggest that diarrhea caused by Vibrio cholerae involves a pro-inflammatory mediators release, such as cytokines, prostaglandin and nitric oxide. The aim of this study was to investigate the role of mast cells and their mediators in the intestinal secretion induced by cholera toxin. We examined the dose responses, time course and role of mast cells and pro-inflammatory mediators in cholera toxin intestinal secretory response, in vivo. Cholera toxin caused a dose-dependent secretion, in ligated small intestine loops, at 18 h. Rats treated with 48/80 compound or ketotifen had a significant decrease in the intestinal secretory response. Cholera toxin secretion was significantly reduced by an unspecific histamine/serotonin receptor antagonist, histamine receptor antagonist, phospholipase A2 and cyclooxygenase inhibitors, platelet-activating factor (PAF) receptor antagonists and TNF-alpha synthesis blockers. On the other hand, pretreatment with a specific serotonin receptor antagonist and lipoxygenase inhibitors failed to block this effect. Analysis of the intestinal fluid from rats injected with cholera toxin, revealed that cholera toxin induces the release of IL-1beta and TNF-alpha into fluid. The data suggest that, at least in part, mast cells are involved in cholera toxin-induced secretion, as well as point to the importance of histamine, prostaglandins, PAF, IL-1beta and TNF-alpha in this process.

Animals↗
PubMed1996

Rice inhibits intestinal secretions.

Rice-based oral rehydration solutions have been found to be effective in decreasing stool output and improving intestinal absorption in acute infectious diarrhea. Recent tests of the ability of a rice extract to inhibit intestinal secretions were undertaken, and it was shown that an isolated fraction of rice extract decreased intestinal losses by actively inhibiting the chloride channel.

Chlorides↗
PubMed2003

Effects of tachykinins and 5-hydroxytryptamine on intestinal secretion.

1. The main aim of the present study was to establish the functional in vivo effects of tachykinins on net fluid transport by the jejunum and ileum of anaesthetized rats. Tachykinins were administered by retrograde infusion in saline into the left common carotid artery. The possible involvement of 5-hydroxytryptamine (5-HT) in tachykinin-induced intestinal secretion was also investigated. 2. Some tachykinins were potent at reversing net absorption to secretion, particularly in the jejunum, where the rank order of potency was neurokinin (NK) A > substance P (SP) > NKB. The potency of the NK1 receptor-selective agonist [Sar9,Met(O2)11]-SP was the same as SP. Neurokinin A reduced net fluid absorption from the lumen of the jejunum at an intra-arterial infusion rate of 0.64 microg/kg per min. Infusions of NKA at 1.6 and 4 microg/kg per min induced net secretion into the lumen of the jejunum. These two higher infusion rates also affected fluid transport by the ileum, although not to the same extent as seen in the jejunum. The relative potency of SP was not affected by captopril (10 mg/kg, i.v.). 3. The secretory response of the jejunum to infusion of 4 microg/kg per min SP was blocked in animals administered the NK1 receptor antagonist SR 140 333 (1 mg/kg, i.v.). In addition, SR 140 333 blocked the secretory response to 4 microg/kg per min NKA. However, NKA still induced secretion in animals that had received the NK2 receptor antagonist SR 48 968 (0.3 mg/kg, i.v.). 4. A role for an endogenous tachykinin in the intestinal secretory action of 5-HT was not clearly established using the present model. Although SR 140 333 increased the absorption rate from the jejunum in animals infused intra-arterially with 5-HT, 5-HT itself did not cause a significant reduction in absorption. There were no significant differences in the absorption rates from the ileum between the control group and groups infused with 5-HT with and without SR 140 333. 5. The present study provides functional evidence for the existence of NK1 receptors in the rat small intestine, particularly in the proximal region, where their activation influences fluid transport. It is suggested that the presently used rat model is suitable for screening tachykinin antagonists for potential antidiarrhoeal activity.

Animals↗
PubMed2005

Angiotensin II subtype 1 receptor blockade inhibits Clostridium difficile toxin A-induced intestinal secretion in a rabbit model.

Angiotensin II (ANG II) has been described in the regulation of intestinal secretion and absorption via angiotensin subtype 1 (AT(1)) and AT(2) receptors, respectively, in rats. We investigated the role that ANG II plays in the rabbit ileal-loop model of Clostridium difficile infection. Expression of AT(1), the more abundant ANG II receptor, was demonstrated in ileal loops, and an AT(1) receptor blocker, losartan, inhibited hypersecretion induced by C. difficile toxin A (mean volume : length ratio, 0.27+/-0.06 vs. 0.60+/-0.06 mL/cm in controls). Losartan also decreased production of ANG II in the ileum (0.48+/-0.06 vs. 0.87+/-0.12 pg/mg in controls), raising the possibility that ANG II may participate in a positive feedback loop involving the hypersecretory response. Our findings suggest that ANG II plays a significant role in the pathogenesis of C. difficile toxin-induced diarrhea.

Angiotensin II↗
PubMed1995

Cholera toxin-induced small intestinal secretion has a secretory effect on the colon of the rat.

BACKGROUND/AIMS: Little information is available on the role of colon during small intestinal secretion. The aim of this study was to examine the effects of secretory changes in the small intestine on the colonic transport of electrolytes and water in vivo. METHODS: The jejunum and colon of the rat were perfused in vivo simultaneously but separately, and jejunal secretion was induced by exposing the jejunum to cholera toxin, 8-bromo-cyclic guanosine monophosphate, or hyperosmolarity. RESULTS: Jejunal perfusion with a hyperosmolar mannitol solution (600 mOsm/L) or with 8-bromo-cyclic guanosine monophosphate (0.5 mmol/L) resulted in net secretion of water in the jejunum but did not affect the baseline rate of water transport in the colon. On the contrary, addition of cholera toxin (1 microgram/loop) to the jejunal segment not only induced a significant local secretory change but also resulted in a similar change in the colon, which was not exposed to cholera toxin. The intestine was transected immediately below the jejunum, thus interrupting the anatomical continuity of the enteric nervous system. This procedure eliminated the distant secretory effect of cholera toxin, thus allowing the conclusion that the enteric nervous system is involved in the distant propagation of the local secretion induced by cholera toxin. CONCLUSIONS: Cholera toxin, but not other secretagogues, triggers a secretory response that is not only local but also extends to distal segments via the enteric nervous system.

Animals↗
PubMedDate not supplied

Effect of quinidine on the intestinal secretion of digoxin in guinea pigs.

Following i.v. injection of digoxin (10 micrograms kg-1) the ratio between digoxin concentrations in the lumen of jejunal loops perfused in situ and in plasma (L/P) of guinea pigs increased linearly with time. After 3 h, L/P was 8.7, indicating net secretion of digoxin against a concentration gradient. In quinidine treated animals (100 mg kg-1 p.o., 2 h before experiment) both the L/P ratio (5.7; p less than 0.01) and the digoxin content of jejunal tissue (-32 per cent; p less than 0.01) were markedly reduced. It is suggested that quinidine reduces the extrarenal clearance of digoxin at least in part by inhibiting the intestinal secretion of this glycoside.

Animals↗
PubMed1997

Peptide YY inhibition of prostaglandin-induced intestinal secretion is haloperidol-sensitive in humans.

BACKGROUND & AIMS: It is uncertain whether peptide YY (PYY) inhibits human intestinal secretion directly through enterocyte receptors or via indirect neural mechanisms. Thus, the effect of PYY on prostaglandin E2 (PGE2)-induced jejunal secretion in normal volunteers was measured, and it was determined whether a dopamine and sigma antagonist affected PYY effect. METHODS: Jejunal absorption of water and electrolytes was measured by a perfusion method in 6 volunteers. A double-blind crossover study was performed, involving intraluminal infusion of PGE2, intravenous infusion of human PYY, and intramuscular injection of haloperidol or placebo. RESULTS: PGE2 induced net secretion of water and electrolytes (P < 0.01 vs. basal). The effect of PGE2 was reduced by about half with 30 pmol x kg(-1) x h(-1) of PYY (plasma PYY, 96 +/- 12 pg/mL) and suppressed by 90 pmol x kg(-1) x h(-1) of PYY (P < 0.01; plasma PYY, 268 +/- 22 pg/mL). Plasma PYY was correlated negatively (P < 0.01) with net fluxes of water, Cl-, Na+, and K+. Haloperidol suppressed the effect of PYY on PGE2-induced secretion (P < 0.05). CONCLUSIONS: PYY administered in doses producing slightly supraphysiological plasma levels inhibits PGE2-induced secretion in normal humans. Sigma or dopamine receptors (probably neuronal ones) are involved in this effect.

Cross-Over Studies↗
PubMed1984

Inhibition by loperamide of deoxycholic acid induced intestinal secretion.

The effect of loperamide on deoxycholic acid (DOC)-induced secretion was studied in ligated loops of the rat jejunum and colon in vivo. In controls, loperamide slightly augmented fluid absorption. 3 mmol DOC caused net fluid secretion. Loperamide reduced this secretion in the colon and reversed it to absorption in the jejunum. Na-K-ATPase specific activity and cAMP levels were measured in the jejunum, and [14C]erythritol clearance as an index of mucosal permeability in the colon. In the jejunum this opiate analogue affected neither basal or DOC-depressed Na-K-ATPase, nor mucosal cAMP. In the colon it reduced a large increase of the erythritol clearance caused by DOC. It is suggested that loperamide interferes with DOC-induced intestinal secretion in part by lowering mucosal permeability.

Animals↗