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At least 1,603 records · Page 89Linked to original sources
PubMed1985

Vasoactive intestinal peptide-containing neurons in the paraventricular nucleus may participate in regulating prolactin secretion.

Vasoactive intestinal polypeptide (VIP) immunoreactivity is present in varicosities and fibers in the hypothalamic paraventricular nucleus (PVN) in normal control animals. Adrenalectomy and lactation combined with colchicine treatment results in the appearance of a large population of VIP-immunopositive cell bodies in the parvocellular part of the PVN. Adrenalectomy, as well as lactation, significantly increases the number of VIP-positive fibers in the external zone of the median eminence. These observations suggest that the VIP-immunopositive neurons in the PVN may participate in regulating prolactin and corticotropin secretion.

Adrenalectomy↗
PubMed2000

Characterization of MPP+ secretion across human intestinal Caco-2 cell monolayers: role of P-glycoprotein and a novel Na(+)-dependent organic cation transport mechanism.

1. In the kidney, a number of transport proteins involved in the secretion of permanently charged organic cations have recently been cloned. To evaluate the possible similarities between intestine and kidney in the handling of organic cations we investigated the transport of 1-methyl-4-phenylpyridinium (MPP+) across monolayers of intestinal Caco-2 cells. MPP+ is a prototypic substrate of the cloned organic cation transporters hOCT1 and hOCT2. 2. In Caco-2 cell monolayers, the basolateral to apical flux of MPP+ was significantly greater than the apical to basolateral flux, consistent with net secretion of MPP+. 3. Net secretion of MPP+ was abolished by addition of either 10 microM cyclosporin A or 100 microM verapamil to the apical membrane. In contrast, secretion of MPP+ was unaffected by addition of either TEA (2 mM) or decynium-22 (2 microM) to either apical or basolateral membranes. These results suggest that MPP+ secretion is mediated primarily by P-glycoprotein located at the apical membrane. We found no evidence of a role for hOCT1 or hOCT2 in the secretion of MPP+. 4. In addition to net secretion of MPP+, we found evidence of a Na(+)-dependent MPP+ uptake mechanism at the apical membrane of Caco-2 cells. 5. Na(+)-dependent MPP+ uptake was sensitive to inhibition by the organic cations; decynium-22 (2 microM), TEA (2 mM) and cimetidine (5 mM) but not by carnitine, guanidine or proline. 6. These results suggest that net secretion of MPP+ across the apical membrane of Caco-2 cells is a function of the relative contributions of MPP+ secretion mediated by P-glycoprotein and MPP+ absorption mediated by a novel Na(+)-dependent transport mechanism.

1-Methyl-4-phenylpyridinium↗
PubMed1978

Analysis of the effects of food and of digestive secretions on the small intestine of the rat: III. Mucosal mass, activity of brush border enzymes, and in vivo absorption of galactose, sodium, and potassium.

A modified Roux-en-y repositioning of rat proximal small intestine resulted in a gut segment (A) exposed only to digestive secretions, but not to food and a gut segment (B) exposed to food, stomach juice and by reflux only to digestive secretions, and a third segment (C) exposed to both, food and digestive secretions. The changes in segment A were qualitatively very similar to those occurring after removal of luminal nutrition (intravenous feeding, self-emptying blind loop, and Thiry Vella loop). These findings support the hypothesis that the presence of luminal nutrition is a major factor regulating mucosal mass and enzyme activity in rat proximal small intestine. The changes in the luminal environment in segment B caused an increase in mucosal mass (in the proximal half only), an increase in sucrase activity which paralleled the increase in mucosal mass, and no change in activity of alkaline phosphatase which in fact was a decrease in activity ;at the cellular level'. Later on the net absorption of sodium and potassium was improved and the disappearance of galactose was unchanged when referred to unit length of small intestine.In segment C there was a small increase in mucosal mass, an increase in activity only for alkaline phosphatase, and an improvement of the net absorption of sodium without changes in the disappearance of galactose. These changes were compatible with a more proximal promotion of a distal gut segment.

Alkaline Phosphatase↗
PubMed1982

Inhibition of pentagastrin-stimulated gastric acid secretion by upper intestinal hyperosmolality in chronic gastric fistula rats.

The effects of upper small intestinal perfusion with iso-osmolar or hyperosmolar polyethylene glycol (PEG) solutions on maximal gastric acid secretion stimulated by intravenous pentagastrin was investigated in Sprague-Dawley rats. The animals were provided with a chronic gastric fistula, a gastroenterostomy and a 4-cm duodenal loop anastomosed end-to-side to the jejunum. The oral end of the duodenal loop was closed and intubated for infusion of various solutions. Saline was infused in the control experiments, 2 ml h-1. In the test experiments, saline was replaced with PEG, 300, 900 or 1,200 mosm.kg-1. Duodenal perfusion with iso-osmolar PEG, 300 mosm-kg-1, did not alter maximal acid secretion. Duodenal perfusion with hyperosmolar PEG 900 or 1,200 mosm.kg-1 significantly inhibited the stimulated 2-hour acid output by 47 and 48% respectively (p less than 0.01). Indomethacin, an inhibitor of the prostaglandin synthesis, did not alter the stimulated acid secretion, and the inhibitory influence on acid secretion of duodenal perfusion with PEG 1,200 mosm.kg-1 as not affected by the drug.

Animals↗
PubMed1992

Both crypt and villus intestinal goblet cells secrete mucin in response to cholinergic stimulation.

Computer-assisted morphometric analysis was used to quantify the effects of cholinergic stimulation on intestinal goblet cells. Within 5 min of stimulation (250 micrograms/kg carbachol sc), many crypt goblet cells were depleted of mucin secretory granules and their apical membranes had the deep cavitation that accompanies recent compound exocytotic activity. The percentage of crypt epithelial volume occupied by mucin secretory granules was decreased by 58.4% at 5 min and 45.9% at 60 min. Although villus goblet cells never showed signs of recent compound exocytosis, morphometric analysis revealed a 22.4% decrease in the percentage of villus epithelial volume occupied by mucin secretory granules within 5 min of stimulation and a 32.4% decrease by 60 min. The decrease in villus mucin stores was due to both a reduction in the volume of mucin in an average villus goblet cell and a drop in the number of recognizable goblet cells per square micrometer of villus epithelium. Mucin stores in both the crypt and villus regions were largely replenished by 4 h poststimulation.

Animals↗
PubMed1979

Effect of purified Escherichia coli heat-stable enterotoxin on intestinal cyclic nucleotide metabolism and fluid secretion.

Enterotoxigenic Escherichia coli cause diarrhea by elaborating two enterotoxins. The large-molecular-weight, heat-labile toxin causes intestinal secretion by stimulating cyclic adenosine 5'-monophosphate production. The mechanism by which the small-molecular-weight, heat-stable enterotoxin induces secretion is unclear. The present study tested the hypothesis that heat-stable enterotoxin induces secretion by altering intestinal cyclic nucleotide concentrations. This was studied in suckling mice by using highly purified E. coli heat-stable enterotoxin obtained from a strain pathogenic for humans. At 3 min after administration of this toxin, intestinal cyclic guanosine 5'-monophosphate (GMP) levels were increased 10-fold. Cyclic GMP levels decreased thereafter, but still were greater than control levels at 120 min. Cyclic adenosine 5'-monophosphate levels fell to one-half of control levels at 3 min and remained below control levels for 120 min. When the time course of enterotoxin-induced secretion was compared with changes in cyclic GMP levels, fluid secretion was not evident until 15 to 30 min after enterotoxin administration. Thus, the increase in intestinal cyclic GMP concentration preceded measurable fluid secretion. And finally, administration of the 8-bromo analog of cyclic GMP evoked fluid secretion, the time course of which was similar to that induced by enterotoxin. These, and other data, strongly suggest that E. coli heat-stable enterotoxin induces intestinal secretion by increasing intestinal cyclic GMP levels.

Animals↗
PubMed1981

Intractable diarrhoea in a patient with vasoactive intestinal peptide-secreting neuroblastoma. Attempted control by somatostatin.

A 1 1/2 year old child developed profuse watery diarrhoea, shown to be due to excessive plasma vasoactive intestinal peptide (VIP) levels, whilst on treatment for metastatic neuroblastoma. Because it was unresponsive to alternative treatment, an attempt was made to control the diarrhoea with a somatostatin infusion. The attempt failed despite the fact that serum VIP levels were substantially reduced. Possible reasons for failure are discussed and the importance of plasma VIP as a marker for maturation in neuroblastoma emphasised.

Diarrhea↗
PubMed1985

Quantitation of sheep IgG1, IgG2, IgA, IgM and albumin by radioimmunoassay.

A solid phase radioimmunoassay procedure for the measurement of immunoglobulins (IgG1, IgG2, IgA and IgM) and albumin in sheep body fluids (serum, intestinal lymph, caudal mediastinal lymph, bile, mammary secretions and intestinal secretions) is described. This method was found to be easy to perform, rapid, sensitive and reproducible. Results obtained were consistent with those previously reported using radial immunodiffusion and nephelometric techniques.

Albumins↗
PubMed1977

Stimulation of insulin and glucagon secretion by vasoactive intestinal peptide.

In vivo, vasoactive intestinal peptide (VIP) produces simultaneous increases in blood glucose and insulin levels. In order to determine whether VIP, like its homologues, also stimulates insulin secretion directly, studies were made in controlled glucose media employing the vascularly perfused cat pancreas. VIP stimulated insulin secretion significantly in the presence of constant physiological concentrations of glucose. The highest insulin response to VIP (100.3+/-8.1 muU/min) approached the highest insulin response to glucose (119.9 +/- 12.0 muU/min). In the absence of glucose, the insulin response to VIP was insignificant. Unexpectedly, VIP was found to be a more effective stimulant of glucagon than of insulin secretion. The highest glucagon response to VIP (327+/-51% of control levels) was attained in the presence of physiological concentrations of glucose and equalled the glucagon response obtained upon withdrawal of glucose from the perfusate. The glucagon response to VIP was blocked by increasing the glucose in the perfusate. These studies indicate the VIP present in pancreatic islets might play a role in the local control of pancreatic endocrine function.

Animals↗
PubMed1997

A new role for enteric glucagon-37: acute stimulation of glucose absorption in rat small intestine.

Glucagon-37 is secreted by intestinal L-cells following carbohydrate uptake. It is known to inhibit gastric acid secretion (hence also named oxyntomodulin) and appears to increase intracellular cyclic AMP concentrations. Since cyclic AMP could enhance intestinal glucose absorption, a possible stimulatory effect of glucagon-37 on glucose transport was examined. Glucagon-37 acutely increased glucose absorption in the isolated, vascularly perfused small intestine and in isolated enterocytes of the rat. In these cells the stimulation by glucagon-37 could be completely blocked by the cAMP antagonist Rp-cAMPS and was therefore mediated by cAMP. The stimulation of intestinal glucose absorption by glucagon-37 appears to be a major new physiological function.

Animals↗
PubMed1987

[Neural regulation of the secretion of the small and large intestines].

The small bowel and the colon are supplied by a dense network of nerves. Nervous control of secretion is influenced by peripheral and central nerves. The small and large intestine are tonically inhibited by the enteric nervous system, in particular by the submucous plexus, to maximally absorb fluid and electrolytes. Choleratoxin induced intestinal secretion may be suppressed by central opiate receptors, and central gamma-aminobutyric acid receptors may inhibit intestinal absorption. Besides the classical neurotransmitters acetylcholine and noradrenalin, which stimulate and inhibit, respectively, secretion, a large number of regulatory peptides and other substances which mainly act as cotransmitters and neuromodulators affect mucosal transport in the small and large intestine. Secretion induced by nerves appears to play a major role in diabetic and infectious diarrhea. The nervous control of secretion in the small and large intestine is an interesting area of current research in intestinal transport. So far already, the results shed new light in a better understanding of intestinal pathophysiology, and they point towards new therapeutic modalities in diarrhea and constipation.

Animals↗
PubMed2006

Chloride-dependent bicarbonate secretion in the mouse large intestine.

The gastrointestinal HCO(3)(-) secretion functions to limit the mucosal acid damage due to HCl secreted in the stomach or organic acids produced in the large intestine. We studied HCO(3)(-) secretion in the mouse large intestine with isolated tissues mounted in chambers by using pH stat method. Addition of Cl(-) to the mucosal side caused an increase in HCO(3)(-) secretion in the cecum and distal colon but had little, if any, effect in the proximal colon. In agreement with this, mucosal surface pH was higher in the cecum and distal colon than in the proximal colon. The Cl(-)-induced HCO(3)(-) secretion in the cecum was inhibited by 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB, mucosal addition), but not by DIDS (mucosal or serosal), acetazolamide, amiloride (serosal) or glibenclamide (mucosal). Removal of Na(+) or addition of propionate had hardly any effect on the Cl(-)-induced HCO(3)(-) secretion. These results suggest that a NPPB-sensitive, DIDS-resistant Cl(-)/ HCO(3)(-) exchanger is present in the apical membrane, and mediates Cl(-)-dependent HCO(3)(-) secretion. This process is probably mainly responsible for the formation of the high pH at the mucosal surface.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1995

Corticosteroids increase procollagen gene expression, synthesis, and secretion by human intestinal smooth muscle cells.

BACKGROUND & AIMS: Collagen synthesis by smooth muscle cells plays an important role in intestinal fibrosis. Corticosteroids inhibit collagen synthesis in fibroblasts. The aim of this study was to examine the effect of corticosteroids on the expression of collagen by human intestinal smooth muscle (HISM) cells in vitro. METHODS: Collagen synthesis was determined by the sensitivity of radiolabeled protein to collagenase. Secretion was determined by polyacrylamide gel electrophoresis of radiolabeled procollagen in the medium. Procollagen messenger RNA was determined by Northern blot analysis. RESULTS: Collagen synthesis by confluent HISM cells was not affected by corticosteroids at 10(-10) to 10(-5) mol/L but, in subconfluent cultures, was nonspecifically increased 50% at 10(-5) mol/L. Procollagen secretion was nonspecifically increased 60% at 10(-6) mol/L dexamethasone without any effect on the type III/I ratio. Procollagen I and III messenger RNA levels responded in a biphasic manner: a 45%-65% increase at 10(-10) mol/L and a 15% and 30% decrease at 10(-8) and 10(-6) mol/L. In fibroblasts, collagen synthesis was inhibited 85% by dexamethasone, procollagen secretion was decreased 70%, the type III/I ratio decreased from 70:1 to 18:1, and procollagen messenger RNA was inhibited 25% and 60% (types I and III). CONCLUSIONS: Collagen expression by HISM cells is refractory to corticosteroids and, at certain concentrations, is augmented.

Blotting, Northern↗
PubMed1982

Crypts are the site of intestinal fluid and electrolyte secretion.

The site of adenosine 3',5'-monophosphate-mediated fluid and electrolyte secretion across mammalian large intestine was found to be the crypts of Lieberkühn by means of two techniques. First, the formation of fluid droplets was visualized on the oil-covered mucosal surface directly over crypt duct openings when secretion was stimulated. Second, microelectrode impalement of individual surface and crypt cells revealed that only crypts cells produced a pattern of secretagogue induced alterations in membrane potential and resistance that was characteristic of secretory epithelia.

Amiloride↗
PubMed1992

Somatostatin does not block the effect of vasoactive intestinal peptide on bile secretion in man.

The effects of intravenously administered somatostatin and vasoactive intestinal peptide (VIP) on bile secretion were studied in 10 patients with complete biliary fistulas. The two peptides were administered both separately and simultaneously. During the infusion of vasoactive intestinal peptide, bile secretion increased by 85%, whereas during somatostatin infusion it decreased by 40%. When the peptides were administered together, the VIP-induced choleretic effect was not reduced by somatostatin. Vasoactive intestinal peptide infusion increased bicarbonate concentration and output, whereas somatostatin had the opposite effect. The output of chloride also increased following vasoactive intestinal peptide infusion but decreased following somatostatin infusion. The concentration of chloride was unaffected by somatostatin whereas it was decreased by vasoactive intestinal peptide. The output of bile acids was unaffected by vasoactive intestinal peptide and decreased by somatostatin infusion, whereas total lipid concentration increased during somatostatin infusion and decreased when vasoactive intestinal peptide was added. It is concluded that, in man, somatostatin acts on the bile acid-dependent canalicular bile secretion and also, to some extent, on the ductular secretion, whereas vasoactive intestinal peptide acts strictly at the ductular level. The effects of the two peptides on bile secretion are independent of each other.

Adult↗
PubMed1983

Effect of spontaneous diabetes on hormone release in BB/Phi rats: comparison between the isolated perfused pancreas/stomach/duodenum/spleen and the isolated perfused pancreas.

We have studied the effects of spontaneous diabetes in BB/Phi rats on hormone release in response to amino acids (15 mM) and to amino acids (15 mM) plus glucose (10 mM) from isolated perfused pancreas/stomach/duodenum/spleen (PSDS) and from isolated perfused pancreas (P) preparations. In the PSDS preparation, diabetes reduced total integrated insulin output by 97% (from 1146 +/- 198 to 40 +/- 24 ng/65 min, P less than 0.001), and glucagon output by about 50% (from 51.6 +/- 13.1 to 24.0 +/- 3.7 ng/65 min, P less than 0.05), whereas somatostatin output did not change (105.5 +/- 48.1 to 110.1 +/- 36.9 ng/65 min). In the P preparation, integrated glucagon output fell by 91% (from 97.9 +/- 26.8 to 8.6 +/- 4.8 ng/65 min, P less than 0.01) whereas integrated somatostatin output more than doubled (from 28.1 +/- 7.5 to 69.6 +/- 14.2 ng/65 min, P less than 0.05). Intestinal glucagon and somatostatin contributions were estimated by comparing hormone release from the PSDS with that from the P preparations. We conclude that in our nondiabetic BB/Phi rats, the pancreas was the only source for the release of glucagon and that the intestinal tract secreted more somatostatin than the pancreas. In the diabetic BB/Phi rats, pancreatic glucagon and insulin release was virtually abolished while glucagon secretion from the intestinal tract increased and somatostatin secretion decreased.

Animals↗