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PubMed1976

Ricinoleic acid effects on rabbit intestine: an ultrastructural study.

In fasting rabbits, segments of ileum and colon were perfused with ricinoleic acid. This fatty acid is the active principle of castor oil and stimulates intestinal fluid secretion. Biopsies taken from perfused segments were examined by electron microscopy after staining with lanthanum hydroxide and ruthenium red. These stains, which typically bind to extracellular surfaces, were used to assess the integrity of junctional zones between cells. In this study, ricinoleate did not alter ruthenium or lanthanum staining in junctional areas, a finding suggesting that ricinoleate does not cause fluid secretion by selectively disrupting these areas.

Animals↗

PubMed1977

Rabbit ileal mucosa exposed to fatty acids, bile acids, and other secretagogues. Scanning electron microscopic appearances.

Segments of rabbit ileum were examined by scanning electron microscopy (SEM) after exposure to various compounds known to stimulate fluid secretion in the small intestine. After perfusion with ricinoleate (castor oil) at a 10 mM concentration, striking changes were observed at villus tips and on the apicolateral surfaces of villi; erosions at tips were confirmed by light microscopy of the same pieces of tissue examined by SEM. The appearances after ricinoleate were reversed in part during perfusion with control buffer for 2 hr. Statistical comparisons between control perfused, treated, and reversal tissues showed that the "damage" produced by ricinoleate, and its reversal, was significant statistically. Tissues treated with other intestinal secretagogues, oleic acid (10 mM), deoxycholic acid (4 mM), cholic acid (4 mM), dioctyl sodium sulfosuccinate (6 mM), and cholera toxin (1 microgram/ml) also showed surface changes by SEM. Fluid secretion, produced by an osmotic agent (mannitol) was not associated with "damage." Changes in structure of the mucosal surface after exposure to intestinal secretagogues should be considered as one possible mechanism of impaired fluid transport.

Animals↗

PubMed1977

[Influence of an injection of chorionic hormone (HCG) on the accumulation of testicular fluid following ligature of the vas deferens in adult Wistar rats].

Using the weight gain of the testis after efferent duct ligation, we have measured the testis fluid secretion. A single injection of HCG to Rats before, at the time or after the ligation leads to three types of effects: no effect which can be explained by the metabolisation of the hormone: a positive and/or a negative one. If the stimulating action of HCG remains unexplained, it must be related with ether anaesthesia. It seems likely that the decrease of testicular fluid secretion may represent the fundamental action of HCG upon the exocrine function of the testis, but the mecanism by which this action occurs remains to be solved.

Animals↗

PubMed1989

Effect of K+ channels in the apical plasma membrane on epithelial secretion based on secondary active Cl- transport.

Models of epithelial salt secretion, involving secondary active transport of Cl- [9], locate the K+ conductance of the plasma membrane exclusively in the basolateral membrane, although there is considerable experimental evidence to show that many secretory epithelia do have a significant apical K+ conductance. We have used an equivalent circuit model to examine the effect of an apical K+ conductance on the composition and flow rate of the fluid secreted by an epithelium in which secretion is driven by the secondary active transport of Cl-. The parameters of the model were chosen to be similar to those measured in the dog tracheal mucosa when stimulated with adrenaline to secrete. We find that placing a K+ conductance in the apical membrane can actually enhance secretion provided the proportion of the total cell K+ conductance in the apical membrane is not greater than about 60%, the enabling effect on secretion being maximal when the proportion is around 10-20%. We also find that even when the entire cell K+ conductance is located in the apical membrane, the secreted fluid remains relatively Na+ rich. Analysis of the sensitivity of model behavior to the choice of values for the parameters shows that the effects of an apical K+ conductance are enhanced by increasing the ratio of the paracellular resistance to the transcellular resistance.

Biological Transport, Active↗

PubMed1987

Enteric nerves mediate the fluid secretory response due to Salmonella typhimurium R5 infection in the rat small intestine.

Eighteen hours after intragastric inoculation Salmonella typhimurium elicited a net fluid secretion in the jejunum and ileum of rats. The mechanisms behind the secretory response were analysed in vivo. Extrinsic denervation of the experimental intestinal segments had no effect. The nerve-blocking agents hexamethonium (i.v.) and lidocaine (serosally applied) blocked the secretion but atropine had no effect. It was demonstrated that the bacteria were invasive by culturing from the intestinal wall. The presence of inflammatory reactions was supported by the facts that i.v. indomethacin blocked the secretory response and that there was an increased capillary leakage of albumin-bound Evans Blue into the interstitium of the intestinal mucosa. There was also a secretory response upon inoculation of the jejunal and ileal segments by cell-free supernatants of broth where bacteria had been cultured for 24 h and thereafter lysed. This response was, however, blocked by i.v. atropine, which had no effect on the secretion elicited by living bacteria. We could show no presence of E. coli LT, ST or cholera toxin in the cell-free supernatant by means of ELISA-tests. We therefore conclude that (1) S. typhimurium R5 invaded the rat jejunal and ileal mucosa, thereby creating an inflammatory response which in turn activated a nerve reflex(es) within the ENS leading to a net fluid secretion; (2) the presence of prostaglandins was needed for activating the reflex(es); (3) the reflex(es) contained a nicotinergic transmission; (4) enterotoxin was of no importance for the secretory response in the model used.

Animals↗

PubMed1999

Chloride channels and salivary gland function.

Fluid and electrolyte transport is driven by transepithelial Cl- movement. The opening of Cl- channels in the apical membrane of salivary gland acinar cells initiates the fluid secretion process, whereas the activation of Cl- channels in both the apical and the basolateral membranes of ductal cells is thought to be necessary for NaCl re-absorption. Saliva formation can be evoked by sympathetic and parasympathetic stimulation. The composition and flow rate vary greatly, depending on the type of stimulation. As many as five classes of Cl- channels with distinct gating mechanisms have been identified in salivary cells. One of these Cl- channels is activated by intracellular Ca2+, while another is gated by cAMP. An increase in the intracellular free Ca2+ concentration is the dominant mechanism triggering fluid secretion from acinar cells, while cAMP may be required for efficient NaCl re-absorption in many ductal cells. In addition to cAMP- and Ca(2+)-gated Cl- channels, agonist-induced changes in membrane potential and cell volume activate different Cl- channels that likely play a role in modulating fluid and electrolyte movement. In this review, the properties of the different types of Cl- currents expressed in salivary gland cells are described, and functions are proposed based on the unique properties of these channels.

Absorption↗

PubMed1996

A receptor decoy inhibits the enterotoxic effects of Clostridium difficile toxin A in rat ileum.

BACKGROUND & AIMS: Clostridium difficile toxin A causes secretion and intestinal inflammation in rodents by binding to a specific trisaccharide Gal alpha 1-3Gal beta 1-4 GlcNAc on enterocyte receptors. The purpose of this study was to explore the ability of Synsorb 90 (Synsorb Biotech Inc., Calgary, Alberta, Canada), and inert support carrying this trisaccharide, to bind toxin A in vitro and to inhibit its enterotoxic effects in vivo. METHODS: Binding of [3H]toxin A to Synsorb 90, Synsorb 83 (beta-mannose attached), and Chromosorb P (inert support with no sugar attached) (Synsorb Biotech Inc.) was measured. The inhibitory effects of these compounds on toxin A-mediated fluid secretion, mannitol permeability, and histological damage were measured in ileal loops in vivo. RESULTS: Toxin A showed specific binding to Synsorb 90, bearing the specific trisaccharide that binds toxin A, but not to Synsorb 83 or to Chromosorb P. Pretreatment of rats with Synsorb 90 by gavage (200 mg/kg body wt), but no Synsorb 83 or Chromosorb P at the same doses, dramatically reduced toxin A-associated fluid secretion and permeability. CONCLUSIONS: An immobilized toxin A receptor sequesters toxin A in the intestinal lumen and inhibits its effects of ileal mucosa. These results suggest a potential use for this agent in treating patients with C. difficile colitis.

Animals↗

PubMed2002

The effect of caffeine on renal epithelial cells from patients with autosomal dominant polycystic kidney disease.

Autosomal dominant polycystic kidney disease (ADPKD) is a hereditary disorder characterized by the progressive enlargement of cysts derived from tubules. Tubule cell proliferation and chloride-dependent fluid accumulation, mechanisms underlying cyst expansion, are accelerated by adenosine 3':5'-cyclic monophosphate (cAMP). This study examined the extent to which caffeine may stimulate the production of cAMP by cyst epithelial cells, thereby adversely increasing proliferation and fluid secretion. Mural epithelial cells from ADPKD cysts and normal human kidney cortex cells (HKC) were cultured, and cAMP levels were determined in response to caffeine and receptor-mediated agonists linked to adenylyl cyclase. Caffeine, a methylxanthine, slightly increased basal levels of cAMP, as did other nonselective phosphodiesterase (PDE) inhibitors, 1-methyl-3- isobutyl xanthine and theophylline and rolipram, a specific PDE IV inhibitor. More importantly, clinically relevant concentrations of caffeine (10 to 50 micro M) potentiated the effects of desmopressin (DDAVP), prostaglandin E(2) (PGE(2)), and isoproterenol to increase cAMP levels in both ADPKD and HKC cells. By contrast, at concentrations that augmented the DDAVP response, caffeine attenuated cAMP accumulation by adenosine, implicating an action apart from the inhibition of PDE. Caffeine enhanced the effect of DDAVP to stimulate transepithelial short-circuit current of polarized ADPKD monolayers, reflecting an increase in chloride secretion. Caffeine potentiated the effect of DDAVP and PGE(2) to increase the levels of phosphorylated extracellular signal-regulated kinase (P-ERK). By contrast, P-ERK levels in HKC cells were not raised by increased intracellular concentrations of cAMP. It is concluded that PDE inhibition by caffeine increases the accumulation of cAMP, and through this mechanism activates the ERK pathway to cellular proliferation and increases transepithelial fluid secretion in ADPKD cystic epithelium. Caffeine is, therefore, a risk factor for the promotion of cyst enlargement in patients with ADPKD.

Caffeine↗

PubMed1999

Effect of the 5-hydroxytryptamine3 (5-HT3)-receptor antagonist KB-R6933 on experimental diarrhea models.

The effects of a 5-hydroxytryptamine3 (5-HT3)-receptor antagonist KB-R6933 (6-amino-5-chloro-1-isopropyl-2-(4-methyl-1-piperazinyl)-benzimidazole dimaleate) on experimental diarrhea and on intestinal fluid secretion stimulated by cholera toxin were examined and compared with those of ramosetron and loperamide. KB-R6933 and ramosetron (0.03-1 mg/kg, p.o.) inhibited the diarrhea induced by 5-HT, but not that by castor oil or prostaglandin E2 (PGE2), in mice. Loperamide significantly inhibited the diarrhea induced by 5-HT, castor oil and PGE2. All drugs tested inhibited the diarrhea induced by restraint stress and the intestinal fluid secretion stimulated by cholera toxin in rats. The results suggest the possibility that KB-R6933 may have clinical efficacy in the treatment of diarrhea.

Animals↗

PubMed1986

Evidence of involvement of the enteric nervous system in the effects of sodium deoxycholate on small-intestinal transepithelial fluid transport and motility.

With an in vivo method, transepithelial net fluid transport and intestinal motility were recorded continuously in rat jejunal segments perfused with a modified Krebs-Henseleit solution with or without the bile salt sodium deoxycholate (4 or 8 mM). The bile salt produced a net fluid secretion and characteristic intestinal contractions. The two effects of the bile salt developed simultaneously and were quantitatively related to each other. Both effects disappeared when the bile salt was removed from the perfusate and diminished when the luminal perfusion was stopped. Hexamethonium (intravenously) and lidocaine (applied topically on the intestinal serosa) inhibited both effects, whereas indomethacin (intravenously) was ineffective. Atropine (intravenously) selectively abolished the intestinal contractions without affecting net fluid transport. Extrinsic denervation of the intestines performed 3 weeks before acute experiments did not influence the results. It is concluded that the bile salt stimulated both fluid secretion and intestinal contractions by activating a local nervous reflex mechanism consisting of a presynaptic cholinergic neuron and two postsynaptic neurons, one of which is cholinergic and innervates the intestinal smooth-muscle cell, and the other of which is noncholinergic and nonadrenergic and innervates the epithelium.

Animals↗

PubMed1994

Enterotoxin Escherichia coli STa activates a nitric oxide-dependent myenteric plexus secretory reflex in the rat ileum.

1. Mucosally added enterotoxin Escherichia coli STa increased the electrogenic Cl- secretion measured as the short-circuit current (Isc) across isolated muscle-stripped and muscle-unstripped rat mid-ilea incubated in vitro. 2. Pretreatment with serosal L-NAME (N omega-nitro-L-arginine methyl ester) or tetrodotoxin (TTX) significantly reduced the maximum Isc and the duration of action of STa in the unstripped but not stripped ilea. D-NAME (serosal), indomethacin or 5-hydroxy-tryptamine-desensitization was ineffective on STa-induced Isc in either stripped or unstripped ilea. 3. Serosal capsaicin reduced the maximum Isc of STa and its duration of action in unstripped ilea. 4. L-Arginine induced a significantly larger increase in the Isc across unstripped ilea than across stripped ilea; this could be significantly reduced by serosal L-NAME or TTX, although these were ineffective in stripped ilea. 5. Pretreatment of anaesthetized rats with I.P. L-NAME suppressed the fluid secretion induced by luminal STa in ilea in vivo but had no effect on that induced by luminal carbachol. 6. Mucosal STa increased electrogenic Cl- secretion across intact rat ileum in vitro by activating a capsaicin-sensitive, nitric oxide-dependent myenteric plexus-mediated secretory reflex. The suppression by L-NAME of STa induced ileal fluid secretion in vivo probably involves the inhibition of this reflex.

Animals↗

PubMed1989

Differences in jejunal and ileal response to E. coli enterotoxin: possible mechanisms.

Escherichia coli, which produce heat-stable enterotoxin (STa), cause intestinal fluid secretion as a mechanism of diarrhea. To determine the factors that modulate the intestinal secretory response, we first compared the time course of the STa-induced secretion in ligated in situ loops of rat jejunum and ileum. We found that the jejunal secretory response was brief (less than or equal to 30 min) while the ileal response to STa was sustained (greater than or equal to 3 h). We then compared the modification of purified STa that occurred in jejunum and ileum and found a close correlation between the continued presence of unmodified, authentic STa and continued fluid secretion in the ligated-loop model. At both sites alteration of STa was demonstrated by high-performance liquid chromatography profile and brush-border membrane binding activity. However, in the jejunum, the modification of STa was qualitatively different and quantitatively much greater. We conclude that the degree to which STa is inactivated or removed from the intestine correlates with the secretory response observed. Inactivation of STa may be a mechanism by which the host limits its secretory response.

Animals↗

PubMed1989

Effects of cholera toxin, Escherichia coli heat stable toxin and sodium deoxycholate on neurotensin release from the ileum in vivo.

Neurotensin (NT) is a biologically active peptide found in specialized epithelial cells (N-cells) in the distal small intestine. In this study we tested the hypothesis that NT may be released by luminal secretagogues, i.e., cholera toxin, Escherichia coli heat-stable toxin and sodium deoxycholate. Cholera toxin elicited net fluid secretion in anesthetized cats. This secretion was accompanied by an increased release of NT-like immunoreactivity (NTLI) into the mesenteric vein when NTLI was measured with either a C-terminally or a N-terminally directed antibody. An increasing plasma NTLI concentration (N-terminally directed antibody) was recorded in the mesenteric vein and femoral artery in cholera experiments. These results indicate that cholera toxin releases NT from the small intestine. Since neurotensin causes intestinal fluid secretion at least in part via an activation of enteric nerves we propose that the N-cell functions as a 'receptor cell' which activates an intramural secretory reflex upon luminal stimulation by cholera toxin. This study does not support a similar role for NT in the secretion elicited by the heat stable toxin of Escherichia coli or by sodium deoxycholate since we were unable to demonstrate any intestinal release of NTLI after exposing the intestine to these secretory agents.

Animals↗

PubMed1997

Combined blockade of 5-HT3- and 5-HT4-serotonin receptors inhibits colonic functions in conscious rats and mice.

We have already reported that 5-hydroxytryptamine3 (5-HT3) receptor antagonists failed to modify 5-HT-accelerated colonic transit in conscious rats, but the 5-HT3 and 5-HT4 receptor dual antagonist FK1052 prevented the enhancement. In this study, the inhibitory effect on the stimulated colonic transit was not also observed with 5-HT4 receptor antagonists (SDZ205-557 and SB204070) in freely moving rats with chronic cannulas implanted into the proximal colon. In contrast, combined antagonism by simultaneous administration of ondansetron and the 5-HT4 receptor antagonist exerted a drastic inhibitory effect on the propulsive motility. Furthermore, we examined the effect of 5-HT receptor antagonists on 5-HT-induced fluid secretion in mice. Although none of these selective 5-HT receptor antagonists (YM060 and ondansetron as 5-HT3 receptor antagonist, SB204070 as 5-HT4 receptor antagonist) by itself produced a great inhibition of the 5-HT-induced diarrhea, the combination of a 5-HT3 receptor antagonist and a 5-HT4 receptor antagonist markedly reduced the diarrhea. These data suggest that 5-HT-accelerated colonic motility and 5-HT-evoked fluid secretion are mediated by both 5-HT3 and 5-HT4 receptors and that the pathways activated by these receptors may collaborate.

4-Aminobenzoic Acid↗

PubMed1978

Effects of dihydroxy bile acids and hydroxy fatty acids on the absorption of oleic acid in the human jejunum.

Perfusion studies of the normal human jejunum were performed to test whether dihydroxy bile acids and hydroxy fatty acids inhibit the absorption of oleic acid, since previous reports documented their inhibitory effects on the absorption of several other organic solutes. 3 mM deoxycholate and 7 mM glycodeoxycholate inhibited the absorption of 3 mM oleic acid in isotonic micellar solutions while inducing net fluid secretion. Similarly, fractional absorption of oleic acid decreased in the presence of hydroxy fatty acids. However, only the changes induced by 2 mM ricinoleic acid could be distinguished from changes induced by an increase in total fatty acid concentration. Under all experimental conditions, close linear relationships existed between net water movement and fractional absorption of glucose, xylose, and fatty acids, as well as between the absorption rates of these solutes. In contrast, net fluid secretion induced by hypertonic D-mannitol (450 mosmol/liter) had no effect on solute absorption. Our data and observations in the literature do not allow formulation of a hypothesis which would adequately define all effects of dihydroxy bile acids and fatty acids on intestinal transport processes. The observations help explain the malabsorption of fat and other nutrients in patients with the blind loop syndrome.

Adult↗

PubMed1988

The initial stages in the action of an insecticidal delta-endotoxin of Bacillus thuringiensis var. israelensis on the epithelial cells of the malpighian tubules of the insect, Rhodnius prolixus.

The effects of the 27 X 10(3) Mr insecticidal delta-endotoxin from Bacillus thuringiensis var. israelensis have been studied using, as a model system, isolated insect Malpighian tubules. At all concentrations of the toxin higher than 1 microgram ml-1 (4 X 10(-8) moll-1) applied to the outer surface of the tubules, fluid secretion failed within about 30 min. Except at very high concentrations, where failure always takes at least 30 s, there was an inverse relationship between the concentration of toxin and the time of failure of toxin-treated tubules. During exposure to toxin, the tubules were initially unaffected for a relatively long period and then rapid failure occurred. If the tubules were removed into toxin-free saline just before failure would have occurred, fluid secretion remained normal for at least 2 h, but on return to the origin toxin-containing saline failure was almost immediate. The toxin was found not to bind to the basement membrane. Ultrastructural changes became evident as tubule failure occurred. These initially involved modifications to the basal side of the cells, but later also to the luminal microvilli. Intercellular junctions became disassociated and cytoplasmic vacuolization occurred. The population of intramembranous particles in the basal membranes became reduced with time. Our findings suggest the following hypothesis for the initial stages in the interaction of the toxin with the tubules. Toxin molecules attach to the accessible cell membranes progressively and irreversibly. They do not readily associate by diffusing laterally in the membrane, so that toxic effects develop only when sufficiently large numbers of them attach close together. The molecules may then associate in some way as a complex, perhaps forming a pore in the membrane. Relatively few such pores lead rapidly to cell failure and death.

Animals↗

PubMed1988

Reserpine treatment increases viscosity of fluid in the epididymis of rats.

Reserpine treatment in rats induces morphological and functional disturbances in exocrine glands which resemble those produced by cystic fibrosis. The general feature is a decrease in fluid secretion with a rise in mucous concentration and altered electrolyte composition. Chronically reserpinized rats have therefore been used as an animal model for the disease. It is known that cystic fibrosis men are infertile due to obstruction of the epididymal duct with inspissated material, a phenomenon that may be secondary to abnormal electrolyte and water transport in the epididymis. Male rats were treated with reserpine (0.5 mg/kg/day) for 12 to 14 days. At the end of the treatment, epididymal fluids were flushed out from the cauda epididymidis for measurement of spermatocrit, viscosity, total protein concentration, sperm concentration and motility. It was found that reserpine treatment caused a rise in viscosity (by 40%), spermatocrit, sperm concentration, and protein concentration. These changes were observed in the epididymis of rats that had been efferent duct-ligated before reserpine treatment. Despite a rise in viscosity of the fluid bathing the spermatozoa, the viability of the stored spermatozoa was apparently normal. Spermatozoa were able to initiate forward motility when suspended in a sodium-containing medium. Testis fluid secretion measured by weight gain after efferent duct ligation for 16 h was not affected by reserpine treatment. The change in viscosity probably was due to a decrease in fluidity in the epididymis. It is concluded that reserpine treatment in rats produced changes in the exocrine functions of the epididymis similar to those seen in other exocrine glands.

Animals↗

PubMed2003

Role of cyclooxygenase enzymes in a murine model of experimental cholera.

Nonsteroidal anti-inflammatory drugs (e.g., indomethacin) inhibit and reduce the fluid secretion responses elicited by cholera toxin (CT), but it has not been conclusively determined which cyclooxygenase (COX) isoform is involved in CT's action. This study evaluated the role of the COX enzymes and their arachidonic acid metabolites in experimental cholera. Swiss-Webster mice were dosed with celecoxib and rofecoxib and challenged with CT in ligated small intestinal loops, and intestinal segments from mice deficient in COX-1 and COX-2 were challenged with CT. The effects of CT on fluid accumulation, prostaglandin E(2) production, mucosal tissue injury, and markers of oxidative stress were measured. Celecoxib and rofecoxib given at 160 micro g per mouse inhibited CT-induced fluid accumulation by 48% and 31%, respectively, but there was no significant difference among cox-1(-/-) and cox-2(-/-) mice in response to CT compared to wild-type controls. CT elevated tissue levels of oxidized glutathione and lipid peroxides and elicited small intestinal tissue injury in two of five cox-1(-/-) and four of five cox-2(-/-) mice. A role for COX-2 in CT's mechanism of action has previously been suggested by the effectiveness of COX-2 inhibitors in reducing CT-induced fluid secretion, but CT challenge of COX-1 and COX-2 knockout mice did not corroborate the pharmacological data. The results of this study show that CT induced oxidative stress in COX-deficient mice and suggest a tissue-protective role for arachidonic acid metabolites in the small intestine against oxidative stress.

Aldehydes↗