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PubMed1986

Involvement of the enteric nervous system in the intestinal secretion induced by sodium deoxycholate and sodium ricinoleate.

Rat small intestine was continuously perfused for up to 3 h with two different concentrations of sodium deoxycholate (4 and 8 mM) or with sodium ricinoleate (6 mM). The 4-mM bile salt solution produced a secretion that developed to a maximal rate within 3 h, whereas the maximal rate was reached within 1 h with the 8-mM bile salt solution. Hexamethonium, a ganglionic blocker, and lidocaine, a local anesthetic, always reduced the net fluid secretion to approximately zero irrespective of the rate of bile-salt-induced secretion, the concentration of the bile salt, or the perfusion time. Fluid secretion induced by sodium ricinoleate was, like the bile-salt-induced secretion, markedly inhibited by hexamethonium and lidocaine but not by atropine. It is concluded that the rate of secretion induced by the bile salt is related to the monomer concentration of free bile salt molecules in close proximity to or within the intestinal epithelium. The intestinal fluid secretion is mainly due to stimulation of an active secretory process via an activation of enteric nerves. Sodium ricinoleate evokes secretion via similar nervous reflex mechanisms.

Animals↗
PubMed2006

Saccharomyces boulardii inhibits ERK1/2 mitogen-activated protein kinase activation both in vitro and in vivo and protects against Clostridium difficile toxin A-induced enteritis.

Saccharomyces boulardii (Sb), a probiotic yeast, protects against intestinal injury and inflammation caused by a wide variety of enteric pathogens, including Clostridium difficile. Given the broad range of protective effects of Sb in multiple gastrointestinal disorders, we hypothesize that Sb modulates host signaling pathways involved in intestinal inflammatory responses. In this study, we found that Sb culture supernatant (SbS) inhibits interleukin-8 production induced by C. difficile toxin A or IL-1beta in human colonocyte NCM460 cells in a dose-dependent fashion. Furthermore, SbS inhibited IL-1beta and toxin A induced Erk1/2 and JNK/SAPK but not p38 activation in NCM460 cells. To test whether this inhibition also occurs in vivo, we used a previously established mouse ileal loop model. On its own, SbS had no significant effect on basal fluid secretion or intestinal histology. However, Erk1/2 activation was significantly inhibited by SbS in toxin A exposed mouse ileal mucosa. In control loops, toxin A increased fluid secretion (2.2-fold), histological score (3.3-fold), and levels of the chemokine KC (4.5-fold). SbS pretreatment completely normalized toxin A mediated fluid secretion (p < 0.01), and histopathologic changes (p < 0.01) and substantially inhibited toxin A-associated KC increases (p < 0.001). In summary, the probiotic yeast S. boulardii inhibits C. difficile toxin A-associated enteritis by blocking the activation of Erk1/2 MAP kinases. This study indicates a new mechanism whereby Sb protects against intestinal inflammation and supports the hypothesis that Sb modulates host inflammatory signaling pathways to exert its beneficial effects.

Animals↗
PubMed1990

Reflex and chemical responses of tracheal submucosal glands in piglets.

In adult animals, airway fluid secretion is enhanced reflexly via central nervous system pathways, and locally by mediators such as substance P. To evaluate the role of maturation on these regulatory mechanisms, we compared the effects of reflex stimulation and intravenous substance P administration on airway secretion in anesthetized, paralyzed and artificially ventilated piglets, 9 to 22 days of age, and older piglets all aged 10 weeks. Airway secretion was monitored by counting the hillocks appearing in the upper trachea in an exposed field of tracheal epithelium (1.2 cm2) coated with powdered tantalum. In younger animals, mechanical stimulation of the larynx had no discernible effect on tracheal submucosal gland secretion. Neither excitation of airway irritant receptors nor stimulation of pulmonary C-fiber receptors by capsaicin caused a significant increase of fluid secretion from tracheal submucosal glands. In addition, stimulation of peripheral chemoreceptors by ventilating animals with 12% O2 in N2, and 6% O2 in N2, failed to induce a substantial change in airway secretion, when compared with number of hillocks in the control period. Furthermore, administration of sodium cyanide had little or no effect on baseline secretion. In contrast, to the weak reflex responses in younger piglets electrical stimulation of the vagus nerve caused the number of hillocks to increase on average by 16.3 +/- 2.3 (P less than 0.01). In addition, local application of a pledget soaked in solution of methacholine caused the number of hillocks to increase by 32.1 +/- 5.2 (P less than 0.01). Intravenous administration of substance P also induced an augmentation in fluid secretion. Increase in concentration of substance P (10(-8), 10(-7), 10(-6), and 10(-5) M, 1 ml) was associated with a concomitant elevation in the number of activated submucosal glands (5.3 +/- 2.6, 10.0 +/- 4.4, 27.1 +/- 4.5, 41 +/- 5). In older piglets, stimulation of laryngeal mucosa, airway irritant receptors, as well as stimulation of pulmonary C-fiber receptors induced a significant increase in tracheal secretion, although stimulation of peripheral chemoreceptors had no effect on airway secretion. These data suggest that reflex responses of submucosal glands are weak during early postnatal development, however, tracheal submucosal glands do respond to exogenously administered cholinergic substances and tachykinin peptides.

Animals↗
PubMed1983

Is the secretagogue effect of deoxycholic acid mediated by the adenylate cyclase-cAMP system.

The role of the adenylate cyclase (Ac)-cAMP system in mediating deoxycholic acid (DOC)-induced fluid secretion was studied in the rat jejunum and colon in vivo using the AC inhibitor, RMI 12 330 A. A potent inhibitory effect of RMI 12 330 A on fluid secretion induced by cholera toxin was demonstrated in ligated rat jejunal loops. On the contrary, the changes of fluid movement in jejunal and colonic loops caused by DOC could not be influenced by RMI 12 330 A, and mucosal cAMP levels of colonic loops were not increased. Colonic mucosal permeability estimated by the 14C-erythritol clearance increased significantly during a 45-min exposure to 3 mmol DOC, and was not affected by RMI 12 330 A. These results do not support the theory that the AC-cAMP system plays an important role in DOC-induced intestinal fluid secretion and suggest that an increase in mucosal permeability is the predominant factor responsible for the secretagogue effect.

Adenylyl Cyclase Inhibitors↗
PubMed1989

Gonadotropin-induced luminal formation in the seminiferous tubules and efferent ductules in young frogs: light and electron microscopic study.

To clarify the mechanism of fluid secretion in the testes at the time of gonadotropin-induced spermiation, young Rana nigromaculata were used. As a morphological index of fluid secretion, luminal formation of the seminiferous tubules, and efferent ductules were observed. The following changes were seen by the administration of hCG or frog pituitary: first, the luminal formation of the seminiferous tubules was seen; next, tubular expansion became evident, and finally, luminal formation and expansion were observed in the efferent ductules. These changes were preceded by the separation of cell contact among Sertoli cells and of cell contact between Sertoli cells and the cells of efferent ductules only in the center and the swelling of Sertoli cells and cells of efferent ductules. With regard to the flow of fluid at the time of spermiation, the present results indicate the possibility that there is a difference in the ability for fluid secretion between Sertoli cells and the ductule cells.

Animals↗
PubMed1996

G protein regulation of alveolar ion channels: implications for lung fluid transport.

Vectorial ion flow across the alveolar epithelium provides the driving force for lung fluid secretion in the prenatal lung and for fluid reabsorption at birth and thereafter into adult life. Fluid secretion is dependent upon 'active' accumulation of Cl- into the lumen of the developing lung and any factor which interupts the production of this liquid template results in life-threatening abnormalities in lung growth. The direction of fluid flow is reversed at birth to bring about the reabsorption of the lung fluid so that gaseous exchange can be initated successfully in the neonate. This functional switch at birth involves active Na+ reabsorption; failure of this mechanism to activate adequately contributes to respiratory distress in the newborn. Although beta 2-adrenoceptor-cAMP-protein kinase activation provides a basic model for the switch, it is clear that local regulation of many of the components in the switching cascade are important to the overall efficiency with which it is achieved. Co-localized with apical Cl- and Na+ channels are pertussis toxin-sensitive G proteins, which exert their regulatory effects principally by direct protein-channel interactions. The modulation of channels by local G proteins is finely tuned by negative feedback mechanisms, which may include a novel double-bond specific fatty acid regulation of G protein turnover and the paracrine effects of locally produced eicosanoids. An understanding of how these overlapping pathways integrate to produce the smooth and ordered transition from Cl- secretion to Na+ absorption will allow the design of rational treatments for conditions that are characterized by disfunctional lung fluid homeostasis.

Age Factors↗
PubMed1998

Identification of a pathogenicity island required for Salmonella enteropathogenicity.

Salmonella spp. interact with ileal mucosa and disrupt normal intestinal function, which results in an acute inflammatory cell influx, fluid secretion and enteritis. We have recently characterized SopB, a novel secreted effector protein of Salmonella dublin, and presented evidence that SopB is translocated into eukaryotic cells via a sip-dependent pathway to promote fluid secretion and inflammatory responses. Here, we show that sopB is located on a large DNA fragment unique to the Salmonella chromosome. This locus is conserved in Salmonella and maps at approximately 20 centisome of the S. typhimurium chromosome. Sequence analysis revealed that this Salmonella-specific DNA fragment is flanked by DNA sequences with significant sequence similarity to the Escherichia coli K-12 genes, tRNA1ser (serT) on one side and copS/copR on the other. Thus, this Salmonella-specific DNA fragment has features characteristic of 'pathogenicity islands' and, therefore, it was denoted SPI-5 (Salmonella pathogenicity island-5). SPI-5 was sequenced and was found to contain five novel genes, pipA, pipB, pipC, pipD (pathogenicity island-encoded proteins) and orf, in addition to sopB. The effect of mutations in pipA, pipB and pipD on the induction of fluid secretion and an acute inflammatory cell influx was assessed in bovine ligated ileal loops. The effect of mutations in SPI-5-encoded genes on systemic salmonellosis was assessed in mice. The results of these experiments suggest that SPI-5-encoded genes contribute to enteric but not to systemic salmonellosis.

Amino Acid Sequence↗
PubMed1994

Alteration of colonic absorption by long-chain unsaturated fatty acids. Influence of hydroxylation and degree of unsaturation.

Unabsorbed dietary unsaturated fatty acids may cause diarrhea in patients with steatorrhea, but their ability to cause colonic fluid secretion is not known. The present study investigated the effect of several dietary long-chain unsaturated fatty acids on colonic absorption and morphology in the rat colon in vivo. The fatty acids tested induced concentration-dependent net water secretion. The ability of these fatty acids to induce net water secretion varied as follows: linolenic acid (18:3) > linoleic acid (18:2), ricinoleic acid (18:1 OH) > oleic acid (18:1), palmitoleic acid (16:1). Net absorption of sodium and chloride were decreased in fatty acid perfusions. Mucosal activity of sodium potassium adenosine triphosphate and adenyl cyclase were not significantly altered by fatty acids. Epithelial cell damage was noted and correlated with the ability of the fatty acid to induce fluid secretion. Unsaturated fatty acids induce epithelial cell damage and fluid secretion in the colon, their effect being related to the degree of unsaturation.

Adenylyl Cyclases↗
PubMed1989

Comparative study of Clostridium difficile toxin A and cholera toxin in rabbit ileum.

The purpose of this study was to compare the effects of Clostridium difficile toxin A and cholera toxin on fluid secretion, intestinal permeability, and arachidonate metabolites in rabbit ileum. Injection of 25 micrograms of either purified toxin into 10-cm ileal loops caused significant increases in fluid secretion and intestinal permeability to mannitol as well as release of prostaglandin E2 into the lumen. Toxin A, but not cholera toxin, caused a severe inflammatory reaction of the lamina propria and necrosis of enterocytes as well as increased release of leukotriene B4. The toxin A-mediated increases in prostaglandin E2 and leukotriene B4 could be blocked by prior instillation of 10 mg of 5-aminosalicylic acid into ileal loops. 5-Aminosalicylic acid also significantly diminished the expected increase in mannitol permeability after both toxins, but had no significant inhibitory effect on fluid secretion or, in the case of toxin A, intestinal inflammation. Our results indicate that C. difficile and cholera enterotoxins differ substantially in their effects on the rabbit intestine. Clostridium difficile toxin A, an inflammatory toxin, produces a striking infiltration of the lamina propria with neutrophils that is associated with increased release of leukotriene B4. In contrast, cholera toxin does not cause inflammation or leukotriene B4 release. Increased release of prostaglandin E2 occurs after exposure to both toxins and appears to be correlated with increased intestinal permeability.

Animals↗
PubMed1988

Effects of acetylcholine, isoprenaline and forskolin on electrolyte and protein composition of rabbit mandibular saliva.

1. The major purpose of this study was to investigate cellular regulation of the ductal transport processes in salivary glands which act to modify the electrolyte composition of primary saliva and cause it to become hypotonic. This was achieved using an isolated mandibular gland preparation by observing the effect of different stimuli on the electrolyte composition of saliva secreted at the same flow rate, on the assumption that these stimuli do not influence primary saliva composition. The effects of the same stimuli on the volume of primary fluid secretion and on protein secretion were also observed. Proteins were measured in total and as individual components after their separation by high-performance liquid chromatography. 2. Acetylcholine was used as a 'Ca2+-mobilizing' agonist (i.e. one which both elevates intracellular Ca2+ concentration and activates protein kinase C). Isoprenaline was initially used to elevate intracellular cyclic AMP concentration but was subsequently abandoned in favour of forskolin. 3. Acetylcholine was a very potent stimulus of primary fluid secretion. By contrast, isoprenaline and forskolin were essentially without effect, even when superimposed on acetylcholine stimulation. 4. As judged by saliva electrolyte composition, increasing the concentration of acetylcholine enhanced ductal absorption of Na+ and Cl- and secretion of K+ (and presumably HCO3-). Forskolin had the opposite effect: when superimposed on submaximal acetylcholine stimulation it caused saliva concentrations of Na+ and Cl- to remain high and K+ low (i.e. it inhibited ductal transport processes). The inhibitory effect of forskolin on ductal transport could be overcome by increasing the concentration of acetylcholine, and vice versa. 5. Acetylcholine, isoprenaline and forskolin each increased salivary protein secretion, although the kinetics of secretion differed. The spectrum of proteins secreted in response to the three stimuli was the same. The relative proportions of the individual proteins was influenced by the strength of stimulation (i.e. the proportions at high total protein output differed from those at low total protein output) but not apparently by the nature of the stimulus. 6. Thus, the three major secretory processes in the rabbit mandibular salivary gland respond differently to the two major signal transduction mechanisms. For primary fluid secretion, Ca2+ is stimulatory and cyclic AMP almost without effect; for ductal transport, Ca2+ is stimulatory and cyclic AMP inhibitory; and for protein secretion both Ca2+ and cyclic AMP are stimulatory.

Acetylcholine↗
PubMed1981

Effects of clanobutin on pancreatic secretion in vitro.

The effects of clanobutin (4-[4-chloro-N-(4-methoxyphenyl)-benzamido]butyric acid) were investigated on two in vitro pancreatic preparations. In rat pancreatic lobules clanobutin (7.2 mM) stimulated the secretion of amylase and radiolabeled proteins to the same or higher extent as did CCK-PZ and carbachol in maximally active doses, but with a delay of 1-2 h. In the isolated rabbit pancreas clanobutin (3.3 mM) stimulated protein secretion about half as much as did carbachol, but without significant delay. The effect of clanobutin on protein secretion was prevented by prior application of carbachol, was not affected by the omission of Ca2+ from the medium and was only partly inhibited by the presence of atropine (0.1 mM). Prior addition of clanobutin did not prevent the effects of carbachol on enzyme secretion. In addition, clanobutin (3.3 mM) inhibited fluid secretion in the rabbit pancreas by about 50 percent; the inhibition was reversible. No effects on paracellular permeability were found with sucrose used as test substance. The findings indicate that clanobutin has opposite effects on enzyme and fluid secretion by rat and rabbit pancreas, which are not due to circulatory effects.

Amylases↗
PubMed1974

A study of intercellular spaces in the rabbit jejunum during acute volume expansion and after treatment with cholera toxin.

The effects of acute volume expansion and of intraluminal administration of cholera toxin have been examined in rabbit jejunum. Acute volume expansion was shown to reverse the normal reabsorptive flux of water and cause significant fluid secretion. Phase and electronmicroscopic examination of the jejunal epithelium showed that marked distension of the intercellular spaces had occurred. Examination of the jejunal epithelium after treatment with cholera toxin showed that, in association with high rates of fluid secretion, the intercellular spaces were extremely small and lateral membranes of adjacent cells were in close apposition to one another. Thus the mechanisms of fluid secretion in these two situations would appear to be quite different. The secretion associated with volume expansion, and accompanied by a rise in venous pressure and bullous deformations of terminal junctions, could well be due to hydrostatic pressure applied through intercellular channels. The secretion of cholera appears to be unrelated to hydrostatic pressure and is more likely due to body-to-lumen active ion transport.

Animals↗
PubMed1984

Intraluminal distension pressure on intestinal lymph flow, serosal transudation and fluid transport in the rat.

Effect of distension pressure (d.p.) on the rate of lymph flow, serosal transudation and fluid transport was studied on an in vivo upper jejunal preparation. In the non-absorptive state with isotonic Na2SO4 solution as the luminal fluid, neither lymph flow nor transudation was increased with increasing d.p. from 0 to 3, 10, 20, 40 or 70 mmHg. Fluid absorption rate (Jv) increased by more than 100% when d.p. was increased from 0 to 3 mmHg whether glucose was present or absent in the luminal fluid (Krebs-Ringer solution). In the presence of glucose, there was no difference in Jv in the range of d.p. between 3 and 70 mmHg. In the absence of glucose Jv decreased when d.p. was above 10 mmHg. Whether with or without glucose, lymph flow did not change between d.p. of 0 and 10 mmHg but decreased at higher pressures. Whether with or without glucose, transudation began to appear at d.p. of 10 mmHg, increased with increasing d.p. up to 70 mmHg, but was much less in the absence of glucose. Protein concentration in the lymph (1.5-2.4% (w/v] and transudation (1.5-2.1% (w/v] was practically the same, suggesting that the latter could have originated from the lymph which leaked out of the serosal membrane. Blood flow in the subserosal capillaries and venules was remarkably reduced when d.p. was above 10 mmHg. In both jejunum and ileum, d.p. never caused fluid secretion during distension but resulted in transient fluid secretion as well as transudation following distension, apparently due to increased capillary filtration as a result of increased capillary permeability by ischaemia (during distension). From the effect of d.p. on the increase of transudation, presumably lymph, it is concluded that luminal hydrostatic pressure may play a role in fluid transport via the lymphatic system.

Animals↗
PubMed1976

Proteinase activity in Ascaris suum eggs, hatching fluid, and excretions-secretions.

Hatching fluid and the excretions and secretions (E.S.) of hatched larvae of Ascaris suum revealed proteinase activity when assayed by 2 different procedures employing collagen or casein as substrates. Both assays apparently detected similar levels of proteinase activity in hatching fluid and E.S. of hatched larvae. The Anson (casein substrate) assay worked best in 0.05 M phosphate buffer, pH 8.0. The Azocoll (collagen substrate) assay worked best in 0.05 M borate buffer at pH 8.8. Azocoll assays done at temperatures ranging from 25 to 65 C revealed maximal proteinase activity at 55 C. Analysis of hatching fluid from 18-, 21-, and 28-day-old embryos and of extracts from sonicated 0- to 28-day-old developmental stages showed that proteinase activity increased markedly 18 days after embryonation had begun. Prior to the 18th day of embryonation proteinase levels were relatively low.

Animals↗
PubMed2003

Isolation, identification and localization of a second beetle antidiuretic peptide.

We isolated from head extracts of Tenebrio molitor a peptide that inhibits fluid secretion by the Malpighian tubules of this insect. This second antidiuretic factor, ADFb, like the previously published ADFa, works through cyclic GMP as a second messenger. It has primary structure Tyr-Asp-Asp-Gly-Ser-Tyr-Lys-Pro-His-Ile-Tyr-Gly-Phe-OH with an EC(50) of approximately 240 pM in a fluid secretion assay. This peptide is now the second sequenced endogenous insect ADF which inhibits Malpighian tubule fluid secretion. Immunohistochemical techniques show that the peptide is localized in the brain; it appears to be produced mainly in two pairs of bilaterally symmetrical cells in the protocerebrum.

Amino Acid Sequence↗
PubMed1984

Absorption and secretion of fluid and electrolytes by the rectum.

Although the amounts of ions and water absorbed and secreted by the rectum are small compared to those of other parts of the colon, rectal epithelium is capable of generating and maintaining considerable ionic gradients. Absorption of Na+ and Cl- and secretion of K+ and HCO-3 leads to relatively low concentrations of the former and high concentrations of the latter within the lumen. Detailed examination of the transport processes indicates that the epithelial mechanisms can be interpreted in terms of ionic movements through transcellular and paracellular pathways. These results show that the epithelium is relatively tight and largely amiloride-sensitive. Active Na+ absorption and apparent active K+ and HCO-3 secretion occur. The secretion of HCO-3 is related to Cl- and organic anion absorption. Mineralocorticoids increase the transepithelial potential difference (p.d.) as well as stimulating Na+ absorption and K+ secretion. Rectal epithelium may, with various physiological or pathological stimuli, become overtly secretory of a predominantly NaCl containing fluid but it remains uncertain whether some secretion is normally present although masked by absorption.

Animals↗
PubMed2003

Circulating ethanol does not stimulate pancreatic secretion in conscious rats.

The purpose of this study was to test the hypothesis that circulating ethanol at concentrations of approximately 0.1 mg% stimulates pancreatic secretion. Awake rats recovered from surgery were used in these experiments. Intravenous infusion protocols were established that produced blood ethanol concentrations 0.1 mg% for over an hour. Maintenance of 0.1 mg% blood ethanol concentration or transient concentrations as high as 0.17 mg% did not cause significant increases in pancreatic protein or fluid secretion. To test whether elevated blood ethanol would augment stimulated pancreatic secretion, the trypsin inhibitor camostat was infused intraduodenally at doses of 0.05, 0.2, and 0.5 mg/hr, each dose level infused for 2 hours. Elevated blood ethanol concentrations (0.1 mg%) did not significantly affect camostat-stimulated pancreatic protein or fluid secretion. In contrast to intravenous infusion, intraduodenal infusion of ethanol significantly stimulated pancreatic protein and fluid secretion, which was associated with blood ethanol concentrations of > or =0.19 mg%. The increases in pancreatic secretion were completely blocked by intravenous infusion of the cholecystokinin (CCK) receptor antagonist CR1409. We conclude that circulating ethanol does not stimulate pancreatic secretion in awake, recovered rats and that intraduodenal ethanol-stimulated pancreatic secretion is mediated by CCK.

Animals↗
PubMed1995

Protein kinase C regulates the magnitude and stability of CFTR currents in pancreatic duct cells.

Activation of protein kinase C (PKC) inhibits adenosine 3',5'-cyclic monophosphate (cAMP)-stimulated fluid secretion in rat pancreatic ducts (N. Ashton, R. L. Evans, and B. E. Argent. J. Physiol. Lond. 452: 99P, 1992). Using the patch-clamp technique, we have investigated whether this inhibition of fluid secretion results from an effect of PKC on cystic fibrosis transmembrane conductance regulator (CFTR) Cl channels. Exposure to 100 nM 4 beta-phorbol 12,13-dibutyrate (PDBu) had no effect on CFTR current density in unstimulated duct cells, but caused a 31% increase in the magnitude of CFTR currents recorded from cells stimulated with cAMP. Furthermore, prolonged (2-4 h) exposure of stimulated duct cells to 100 nM PDBu (a condition that should downregulate PKC) significantly slowed the rate at which CFTR currents run down after establishing a whole cell recording. A similar effect was observed with calphostin C (500 nM), a specific inhibitor of PKC. Thus, although inhibition of ductal fluid secretion by PDBu is unlikely to be explained by an effect on CFTR, modulation of PKC activity can affect both the magnitude and stability of CFTR currents in pancreatic duct cells.

Animals↗