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At least 1,765 records · Page 98Linked to original sources
PubMed1992

Isolation and bioactivity of putative cholecystokinin-releasing peptide from rat small intestinal mucosa.

Pancreatic exocrine secretion in the conscious rat is regulated by proteases in the intestine secreted by the pancreas, and cholecystokinin (CCK) is known to be involved in the mechanism. The authors proposed that the release of CCK was regulated by a CCK-releasing factor secreted into the intestinal lumen from the proximal intestine. We isolated and partially purified a CCK-releasing factor from rat small intestine by gel filtration and high performance liquid chromatography. The partially purified CCK-releasing factor increased pancreatic exocrine secretions and plasma CCK concentrations in conscious rats and this activity was abolished after the incubation with trypsin. The bioactivity of the partially purified CCK-releasing factor was confirmed.

Animals↗
PubMed1989

Quantification of antigen-specific antibody-secreting cells in the small intestine and other lymphoid organs of mice after oral booster immunization.

The intestinal immune response of mice against ovalbumin (OVA) was quantified by isolating lymphoid cells from the small intestine (SI) and testing them for antigen-specific immunoglobulin (Ig) secretion. The isolation procedure for functionally active lymphoid cells from the SI, originally developed to quantify the number of 'background' Ig-secreting cells in the SI, proved to be a useful method for evaluating antigen-specific intestinal immune responses quantitatively. The method was able to detect antigen-specific antibody-secreting cells (ASC) in the SI even when these cells occurred at a minimum frequency of only 0.006%. When mice were primed intraperitoneally (i.p.) with polymerized OVA and given an oral OVA booster immunization, OVA-specific ASC appeared in the SI from Day 3 after booster. After i.p. priming and an i.p. booster these cells could not be detected in the SI. The OVA-specific IgA-ASC responses in various organs after oral booster immunization were compared. From Day 5 after booster, when the response peaked, most OVA-specific IgA-ASC occurred in the SI. This suggested that these cells are mainly responsible for the OVA-specific antibodies demonstrated by ELISA in intestinal secretions from Day 6 after oral booster immunization. It is concluded that the quantitative method used in this study detects antigen-specific ASC in the SI with great sensitivity and could be used to evaluate immunization regimes aimed at inducing intestinal mucosal immune responses.

Animals↗
PubMed1991

Link between cell apical morphology and H+ secretion in salamander small intestine.

To determine the morphological basis for the cellular secretion of H+ by in vitro salamander jejunum the transepithelial proton flux (JH) was measured under different conditions and compared with the ultrastructure of the villus absorptive cells using transmission electron microscopy in conjunction with morphometric analysis. Norepinephrine (NE) stimulated JH and significantly increased the density of small cytoplasmic vesicular and tubular profiles in the region immediately below the apical plasma membrane of the absorptive cells. Cytoplasmic tubular elements were often observed in direct contact with the plasma membrane at the base of the microvilli, suggesting that expansion of the plasma membrane had occurred. The alpha 2-antagonist, yohimbine, blocked NE-stimulated H+ secretion and reduced the number of tubulovesicles. Theophylline reduced the rate of spontaneous acid secretion and the density of apical tubules and vesicles. Exposure to horseradish peroxidase revealed a physical connection between the extracellular space and the apical tubulovesicular compartment. The direct relationship between the number of apical vesicular and tubular profiles and JH suggests that the luminal membrane plays a fundamental role in the cellular events in H+ secretion. The membranes of the tubules and vesicles may be elements of a dynamic pool of transporting membranes under the control of exogenous effectors such as catecholamines.

Animals↗
PubMed1975

The intestinal phase of gastric secretion: a pharmacological profile of entero-oxyntin.

In dogs with denervated fundic pouches, antrectomy, and gastrojejunostomy, feeding a meal of cooked liver and 5 percent bone dust stimualted acid secretion from the fundic pouches without increasing serum gastrin concentrations. Simultaneous administration of pentagastrin, histamine, octapeptide of cholecystokinin, or bethanecol produced potentiation of acid secretion, suggesting that the mediator of the intestinal phase is different from these secretagogues. Secretin and glucagon failed to inhibit the intestinal stimulus but both atropine and metiamide were potent inhibitors. We conclude that entero-oxyntin, the hormone responsible for the intestinal phase of gastric secretin, has a unique pattern of effects for acid secretion.

Animals↗
PubMed2002

Vasoactive intestinal peptide-stimulated Cl- secretion: activation of cAMP-dependent K+ channels.

Vasoactive intestinal peptide (VIP) stimulates active Cl- secretion by the intestinal epithelium, a process that depends upon the maintenance of a favorable electrical driving force established by a basolateral membrane K+ conductance. To demonstrate the role of this K- conductance, we measured short-circuit current (I(SC)) across monolayers of the human colonic secretory cell line, T84. The serosal application of VIP (50 nM) increased I(SC) from 3 +/- 0.4 microA/cm2 to 75 +/- 11 microA/cm2 (n = 4), which was reduced to a near zero value by serosal applications of Ba2+ (5 mM). The chromanol, 293B (100 microM), reduced I(SC) by 74%, but charybdotoxin (CTX, 50 nM) had no effect. We used the whole-cell voltage-clamp technique to determine whether the K+ conductance is regulated by cAMP-dependent phosphorylation in isolated cells. VIP (300 nM) activated K+ current (131 +/- 26 pA, n = 15) when membrane potential was held at the Cl- equilibrium potential (E(Cl-) = -2 mV), and activated inward current (179 +/- 28 pA, n = 15) when membrane potential was held at the K+ equilibrium potential (E(K+) = -80 mV); however, when the cAMP-dependent kinase (PKA) inhibitor, PKI (100 nM), was added to patch pipettes, VIP failed to stimulate these currents. Barium (Ba2+ , 5 mM), but not 293B, blocked this K+ conductance in single cells. We used the cell-attached membrane patch under conditions that favor K + current flow to demonstrate the channels that underlie this K+ conductance. VIP activated inwardly rectifying channel currents in this configuration. Additionally, we used fura-2AM to show that VIP does not alter the intracellular Ca2+ concentration, [Ca2 +]i. Caffeine (5 mM), a phosphodiesterase inhibitor, also stimulated K+ current (185 +/- 56 pA, n = 8) without altering [Ca2+]i. These results demonstrate that VIP activates a basolateral membrane K+ conductance in T84 cells that is regulated by cAMP-dependent phosphorylation.

Caffeine↗
PubMed1997

Heterogeneity of 5-HT receptors mediating secretion in the human intestine.

In conclusion, application of 5-HT has been shown to induce fluid secretion in both the small and large intestine of man. By the use of selective antagonists, the receptors mediating these effects have been identified and characterized. 5-HT induces secretion across human ileal mucosa via a receptor of the 5-HT4 sub-type, whereas a receptor of the 5-HT2A sub-type appears to mediate the effect in human sigmoid colon. The response in human ascending colonic mucosa cannot be definitively classified at this time, but may reflect the presence of a heterogenous receptor population.

Humans↗
PubMed1988

Stimulatory effect of vasoactive intestinal polypeptide on catecholamine secretion from isolated guinea pig adrenal chromaffin cells.

The stimulatory effect of vasoactive intestinal polypeptide (VIP) on catecholamine (CA) secretion from isolated guinea pig adrenal chromaffin cell was studied. VIP (1-10 microM) induced dose-dependent CA secretion, which was slow and continued for at least 30 min. This VIP-induced CA secretion was dependent on the presence of Ca2+ in the medium, but no significant increase in Ca2+ uptake by the cells was observed during their stimulation with VIP. Studies on the intracellular free Ca2+ level ([Ca2+]i) using fura-2 showed that acetylcholine and muscarine induced a marked increase in the [Ca2+]i, but that VIP induced only a slight increase. Thus VIP may induce CA secretion by increasing the sensitivity of the secretion of CA to Ca2+.

Adrenal Medulla↗
PubMedDate not supplied

[Surgical correction of disorders of intestinal phases of gastric secretion in the treatment of peptic ulcer and its complications].

Shown in the paper is a possibility of surgical correction of disturbances in the intestinal phase of gastric secretion in treating peptic ulcer and its complications which are encountered in an overwhelming majority of patients. Sympathectomy of relevant vascular trees is regarded as a pathogenetically validated procedure as is correction of duodenal motility combined with selective proximal vagotomy and excision of the ulcer. It is shown that truncal and selective vagotomy can aggravate the existing disorders of the intestinal phase of gastric secretion.

Gastric Acid↗
PubMed1988

Influence of digestive secretions and food on intestinal absorption of nicardipine.

The role of digestive absorption in the pharmacokinetics of nicardipine has been studied by the perfusion technique. Nicardipine (40 mg) was perfused in six healthy subjects at 5 ml/min for 2 h either in isotonic saline with (Experiment A) or without (B) an occlusive balloon isolating the test segment from digestive secretions, or in a nutrient solution (Experiment C). In Experiments A and B, 100% of nicardipine was absorbed from the jejunal lumen in a 25 cm test segment and in Experiment C it was slightly lower (94%). There was no relationship between the absorption of nicardipine and water movement or bile salt concentration in the jejunum. Nicardipine was already present in the first plasma sample taken after 15 min and the peak level was found at the end of the perfusion. The areas under the curves differed widely between subjects, because of interindividual variation in the first pass effect, but they were similar in Experiments A, B and C. The experimental data showed a good fit to a mode involving a two-phase absorption process. The first phase was associated with intestinal perfusion (zero order process) and the second with passage across the intestinal wall (1st order process). In three further healthy subjects, nicardipine in saline was perfused in the jejunum and then in the ileum on consecutive days. Mean plasma levels over time were similar. The study showed that absorption of nicardipine both from the jejunum and the ileum was complete and was especially rapid. The food-induced change in the kinetics of absorption from the jejunum was too small to affect the pharmacokinetic parameters of nicardipine.

Adult↗
PubMed1989

Effect of VIP antagonist on VIP-, PGE2-, and acid-stimulated duodenal bicarbonate secretion.

Vasoactive intestinal peptide (VIP), prostaglandin E2 (PGE2), and luminal acidification are each potent stimulants of duodenal mucosal bicarbonate secretion. The present experiments were performed to determine whether the recently described VIP antagonist, [4Cl-D-Phe6,Leu17]VIP, suppresses VIP-stimulated duodenal mucosal bicarbonate secretion and to determine whether VIP serves as a mediator of bicarbonate secretion stimulated by acid or PGE2. In anesthetized rats, the effects of intravenous VIP, intraluminal PGE2, and intraluminal HCl on duodenal mucosal bicarbonate secretion both in the presence and absence of [4Cl-D-Phe6,Leu17]VIP were measured. The VIP antagonist inhibited duodenal bicarbonate secretion stimulated by both intravenous VIP and luminal acidification but not luminal PGE2. These findings suggest that VIP could be one mediator of acid-induced duodenal bicarbonate secretion and that the mechanism of PGE2-stimulated bicarbonate secretion is independent of VIP.

Animals↗
PubMed2004

Intestinal absorption and biliary secretion of zinc in rats with chronic renal failure.

BACKGROUND/AIMS: In chronic renal failure (CRF), zinc deficiency is partially attributed to decreased intestinal zinc absorption, but the mechanism of this decrease in intestinal zinc absorption is obscure. Therefore, the objective of this study was to investigate the cause of decreased intestinal zinc absorption in a uremic rat model using an in vivo perfusion technique as well as to evaluate the effect of intestinal zinc perfusion on the secretion of biliary zinc in normal and CRF rats. METHODS: CRF was induced by five-sixths nephrectomy (Nx). During zinc sulfate perfusion, absorption of zinc in the small intestine and the response of plasma zinc level were measured. After intestinal zinc perfusion for 80 min, the concentrations of zinc and metallothionein (MT) in the intestinal mucosal and liver tissue were assayed. The secretion of biliary zinc and the excretion of urinary zinc were also determined before and after zinc sulfate perfusion. The results were compared with those obtained from 10 sham-operated normal rats. RESULTS: The CRF rats showed a significant decrease in the rate of intestinal zinc absorption and in the response of plasma zinc levels during intestinal zinc perfusion. They also had significantly higher levels of mucosal zinc and MT than sham-operated normal rats, but their contents of liver zinc were significantly lower than those of sham-operated normal rats after zinc sulfate perfusion. CRF rats showed a low plasma zinc level and a high urinary zinc excretion in baseline levels, but had similar output of basal biliary zinc as compared with sham-operated normal rats. Zinc sulfate perfusion in the small intestinal was not found to increase the secretion of biliary zinc and the excretion of urinary zinc, either in normal or CRF rats. CONCLUSION: In the CRF rat, the reduction of intestinal zinc absorption may result from reduced mucosal zinc efflux from the basolateral membrane into plasma. These data also suggest that the absorbed zinc from the gastrointestinal tract is mostly taken up by the liver or other tissues, and is less excreted in bile juice and urine.

Animals↗
PubMed1976

Cyclic AMP and bicarbonate responses of the dog pancreas to vasoactive intestinal peptide (VIP) and secretion.

The effects of secretin (3 CU per kilogram) and vasoactive intestinal peptide (VIP; 8 mug per kilogram) on bicarbonate and cyclic AMP secretions in pancreatic juice (with pancreatic duct perfusion) and on pancreatic tissue cyclic AMP were investigated as a function of time in 13 anesthetized dogs. The peptides were given by rapid intravenous injection. Even 30 sec. after peptide administration, tissue cyclic AMP levels were elevated, reaching peak values within the first minute and a second peak at about 3 min. Bicarbonate and cyclic AMP secretions in pancreatic juice started with a lag of 1 min. after peptide injection. Following the injection of VIP, peak pancreatic response developed within the first 5 min. and the pancreatic response actually disappeared after 15 min., whereas secretion evoked by secretin was sustained for at least 30 min. The mean +/- S.D. observed maximal bicarbonate response to VIP (100 +/- 49 muEq./5 min.) was about one sixth of the maximum output following secretin (592 +/- 181 muEq./5 min.). Increases in pancreatic tissue and juice cyclic AMP caused by VIP were significant (p less than 0.05) at 1 and 4 min.; however, they were but moderate if compared with the rise achieved by secretin. The results presented confirm previous reports that VIP is a secretin-like partial agonist of pancreatic bicarbonate secretion and are compatible with the hypothesis that both secretin and VIP elicit canine pancreatic bicarbonate secretion via the second messenger system of cyclic AMP.

Animals↗
PubMed1992

Relationship between intestinal function and chloride secretion in patients with cystic fibrosis.

Cystic fibrosis (CF) is the most frequent inheritable disease with a lethal course. One of the major problems of the disease is malabsorption and malnutrition, due to pancreatic insufficiency which is already present at birth in more than 85% of the patients. Characteristically the mucoid secretion products of the epithelial tissues in lung, pancreas, liver and intestine have a high viscosity. The pathophysiology is characterized by obstruction of these organs with secondary damage and finally destruction. For a long period intestinal obstruction syndromes in CF were ascribed only to the pancreatic insufficiency. Malabsorption is not only caused by enzyme deficiency but is also related to transport processes to the surface of the enterocytes. This indicates that the intestinal disorders in CF are partly the result of mucoid plugging and not only of pancreatic insufficiency. Recently in vitro studies have shown a blockade of secretion through chloride channels in the mucosal membrane of CF tissues. In vivo measurements of chloride fluxes in the rectum showed a disturbed regulation in CF patients. The high viscosity of the mucus and plugging is directly related to the diminished chloride secretion. So it is postulated that the abnormal chloride secretion is responsible for the intestinal obstruction and partially also for the malabsorption.

Chlorides↗
PubMed1997

Antisecretory factor suppresses intestinal inflammation and hypersecretion.

BACKGROUND: Antisecretory factor (AF) is a recently identified regulatory protein which inhibits the intestinal fluid secretion induced by cholera toxin. AIMS: To test the effect of AF on: (a) inflammation and hypersecretion induced by toxin A from Clostridium difficile; and (b) morphological changes and hypersecretion induced by okadaic acid (the blue mussel toxin) in rat intestinal mucosa. METHODS: Morphological changes and fluid accumulation were observed in intestinal loops challenged with 1 microgram of toxin A or 3 micrograms of okadaic acid administered before or after injection of 0.1 microgram of recombinant AF (rAF). RESULTS: The cytotoxic and inflammatory reaction caused by toxin A was abolished after treatment with rAF given either intraveneously or intraluminally prior to the toxin or one hour after the toxin. The intestinal fluid response induced by toxin A and okadaic acid was reduced 55-80% by rAF. However, the characteristic increase in goblet cells at the tips of villi in the okadaic acid treated mucosa was not inhibited by rAF. CONCLUSION: Results suggest that AF might be involved in protection against inflammation and in counteracting dehydration caused by enterotoxins. Both effects are probably mediated via the enteric nervous system.

Animals↗
PubMed2000

Medium- and long-chain fatty acids differentially modulate interleukin-8 secretion in human fetal intestinal epithelial cells.

The primary therapeutic effects of enteral nutrition in patients with Crohn's disease have been reported previously. Although the quantity and type of fat in enteral nutrition are considered to be important, it is unclear how fat modulates mucosal inflammatory responses in the intestine. In the present study, we evaluated the effects of medium-chain and long-chain fatty acids (MCFA and LCFA) on interleukin (IL)-8 secretion in a fetal intestinal epithelial cell line, intestine-407 cells. IL-8 expression was evaluated at the protein and mRNA levels. The activation of nuclear factor-kappaB was assessed with an electrophoretic gel mobility shift assay. The addition of oleic acid (LCFA) micelles, but not octanoic acid (MCFA) micelles, weakly but significantly enhanced basal IL-8 secretion in the intestine-407 cells. The addition of MCFA (5 mmol/L) induced a 40% increase in IL-1beta-induced IL-8 secretion and a 35% increase in tumor necrosis factor (TNF)-alpha-induced IL-8 secretion, respectively. The addition of LCFA (5 mmol/L) induced a 140% increase in IL-1beta-induced IL-8 secretion and a 110% increase in TNF-alpha-induced IL-8 secretion, respectively. These responses were also observed at the mRNA levels. The electrophoretic gel mobility shift assay indicated that both MCFA and LCFA enhanced IL-1beta- and TNF-alpha-induced nuclear factor-kappaB activation. We demonstrated the proinflammatory activities of MCFA and especially LCFA. It is likely that medium-chain triglycerides may be more suitable than long-chain triglycerides as an energy source in enteral diets in the treatment of patients with Crohn's disease.

Cells, Cultured↗
PubMed1986

Studies on the secretion of amino acids and of urea into the gastro intestinal tract of pigs. 2. Net secretion of leucine into the small and large intestines.

The experiment was carried out on 3 pigs of 34 kg body weight equipped with re-entrant cannulas both in the duodenum and terminal ileum. Furthermore, catheters were inserted into the external jugular vein and into the carotid artery. During a preliminary period digesta from both cannulas were collected and stored. This digesta was than reintroduced during a 12 hours period of intravenous infusion of 14C-leucine while outflowing digesta from the proximal parts of the cannulas were collected, stored and analyzed for leucine content, 14C-radioactivity and specific radioactivity of leucine. This paper reports the net secretion of 14C-activity and of 14C-leucine by the small intestine and the recovery of both in the content of the digestive tract at the end of the infusion. It was concluded that endogenous leucine enters the lumen of the small intestine through the intestinal wall mainly in a protein bound form. Free leucine is secreted, however, only in small amounts. Metabolites of leucine were also secreted into or formed in the lumen of the small intestine. A proportion of endogenous leucine was reabsorbed during the passage of digesta along the small intestine.

Amino Acids↗