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PubMed1993

Adaptive cytoprotection of the rat duodenum is not dependent on nitric oxide-induced changes in blood flow.

Mild irritation of the rat duodenum enhances mucosal resistance to acid via a prostaglandin-mediated mechanism. Prostaglandins increase mucosal blood flow, but it is not known whether such changes in blood flow significantly contribute to adaptive cytoprotection. We induced blood flow changes by manipulating the arginine-nitric oxide pathway, which is independent from prostaglandin synthesis, and determined the resulting effects on the cytoprotective response. In anesthetized rats, we tested the effects of intraduodenal infusion of mild acid on duodenal blood flow and on the prevention of mucosal damage by subsequent strong acid in control, indomethacin-pretreated, and NG-nitro-L-arginine-pretreated rats (NG-nitro-L-arginine inhibits the nitric oxide synthase). Additional experiments tested the effects of the prostaglandin analogue 16,16-dimethyl-prostaglandin (PG) E2 or sodium nitroprusside (nitric oxide donor) on duodenal blood flow and on mucosal protection against acid. Exposure of the duodenal mucosa to mild acid increased duodenal blood flow and mucosal resistance to acid. Instillation of 16,16-dimethyl-PGE2 also increased blood flow and mucosal resistance to acid. However, sodium nitroprusside increased blood flow without increasing mucosal resistance to acid, and NG-nitro-L-arginine inhibited the change in blood flow induced by acid while preserving the adaptive cytoprotection phenomenon intact. In conclusion, adaptive cytoprotection of the duodenal mucosa appears to be independent of changes in blood flow.

16,16-Dimethylprostaglandin E2↗
PubMed1994

Na-K-Cl cotransport in villus and crypt cells from rat duodenum.

The aim of the present study was to examine the possibility that Cl- uptake into both villus and crypt epithelial cells of rat duodenum occurs via an electroneutral Na-K-Cl coupled-transport mechanism. Sheets of villus cells and whole crypts were isolated using a Ca2+ chelation technique combined with continuous vibration at low temperatures. Structurally intact, viable epithelia from defined regions along the villus-crypt axis were produced. Uptake of 86Rb+ (as a proxy for K+) into both villus and crypt cells appeared to depend on a coupled process, as evidenced by the inhibition of 86Rb+ uptake by bumetanide and by the removal of either Na+ or Cl- from the bathing media. We report an improved method of isolation of viable enterocytes from defined regions along the villus-crypt axis. We demonstrate the presence of Na-K-Cl cotransport in both villus and crypt duodenal enterocytes.

Animals↗
PubMed1996

Defective iron uptake by the duodenum of Belgrade rats fed diets of different iron contents.

Homozygous Belgrade rats have an inherited hypochromic, microcytic anemia that is due to impaired iron transport into immature erythrocytes. There is also evidence for abnormal iron transport in other tissues such as the intestine. This study was aimed at investigating the intestinal defect in rats that had been fed diets for 12 days that are normal, low, or high in iron. The duodenal uptake, transfer, and absorption of Fe(III)-nitrilotriacetate and Fe(II)-ascorbate were studied using in vivo tied-off gut sacs in genetically normal rats and in heterozygous or homozygous Belgrade rats. In normal and heterozygous Belgrade rats, the handling of Fe(III) and Fe(II) was similar; uptake, transfer, and absorption of Fe(III) and Fe(II) changed inversely with the iron content of the diet. In contrast, in homozygous Belgrade rats the uptake of both Fe(III) and Fe(II) was markedly reduced and absorption of Fe(III) did not change when animals were fed an iron-deficient diet. Since absorption of Fe(II) was similar to Fe(III), there is no evidence that the defect in iron absorption is due to failure of a mechanism for reduction of Fe(III). The lowered uptake of Fe(III) and Fe(II) in homozygous Belgrade rats probably involves a defective iron carrier associated with the microvillous membrane of the duodenum.

Absorption↗
PubMed1998

Effect of VIP and PACAP on basal release of serotonin from isolated vascularly and luminally perfused rat duodenum.

The effect of vasoactive intestinal polypeptide (VIP), pituitary adenylate cyclase-activating peptide-38 (PACAP-38), and PACAP-27 on the release of serotonin (5-HT) into the intestinal lumen and the portal circulation was studied by using in vivo isolated vascularly and luminally perfused rat duodenum. 5-HT levels were determined by HPLC. VIP, PACAP-38, and PACAP-27 reduced the luminal release of 5-HT but did not affect the vascular release of 5-HT. The inhibitory effect caused by VIP, PACAP-38, and PACAP-27 was not affected by either atropine, hexamethonium, TTX, or TTX plus ACh, but it was completely antagonized by the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine (L-NNA). The VIP receptor antagonist VIP-(10-28) blocked the effects of VIP, PACAP-38, and PACAP-27. These results suggest that VIP and PACAP exert a direct inhibitory effect on the luminal release of 5-HT from the enterochromaffin (EC) cells via a common receptor site on the EC cells and that this effect is mediated by NO but not by cholinergic pathways. A single injection of TTX, atropine, or hexamethonium reduced the luminal release of 5-HT, whereas a single injection of VIP-(10-28) stimulated the luminal release of 5-HT and this effect was antagonized by atropine, hexamethonium, or TTX. These results suggest that EC cells may receive the direct innervation of cholinergic neurons as well as VIP and/or PACAP neurons, with the former exerting a tonic stimulatory influence and the latter exerting a tonic inhibitory influence on 5-HT release into the intestinal lumen.

Acetylcholine↗
PubMed1999

Acid-sensing pathways of rat duodenum.

We tested the hypothesis that the duodenal hyperemic response to acid occurs through activation of capsaicin-sensitive afferent nerves with subsequent release of vasodilatory substances such as calcitonin gene-related peptide (CGRP) and nitric oxide (NO). Laser-Doppler flowmetry was used to measure duodenal blood flow in urethan-anesthetized rats. Duodenal mucosa was superfused with pH 7. 0 buffer with capsaicin or bradykinin or was acid challenged with pH 2.2 solution, with or without vanilloid receptor antagonists, a CGRP receptor antagonist, an NO synthase (NOS) inhibitor, or a cyclooxygenase inhibitor. The selective vanilloid receptor antagonist capsazepine (CPZ) dose dependently inhibited the hyperemic response to acid and capsaicin but did not affect bradykinin-induced hyperemia. Ruthenium red was less inhibitory than capsazepine. Selective ablation of capsaicin-sensitive nerves, CGRP-(8-37), and N(G)-nitro-L-arginine methyl ester inhibited acid-induced hyperemia, but indomethacin did not. We conclude that luminal acid, but not bradykinin, stimulates CPZ-sensitive receptors on capsaicin-sensitive afferent nerves of rat duodenum. Activation of these receptors produces vasodilation via the CGRP-NO pathway but not via the cyclooxygenase pathway. Acid appears to be the endogenous ligand for duodenal vanilloid receptors.

Acids↗
PubMed2000

A novel in vitro model of Brunner's gland secretion in the guinea pig duodenum.

A novel in vitro model that combined functional and morphological techniques was employed to directly examine pathways regulating Brunner's gland secretion in isolation from epithelium. In vitro submucosal preparations were dissected from guinea pig duodenum. A videomicroscopy technique was used to measure changes in luminal diameter of glandular acini as an index of activation of secretion. Carbachol elicited concentration-dependent dilations of the lumen (EC(50) = 2 microM) by activating muscarinic receptors on acinar cells. Ultrastructural and histological analyses demonstrated that dilation was accompanied by single and compound exocytosis of mucin-containing granules and the accumulation of mucoid material within the lumen. Inflammatory mediators (histamine, PGE(1), PGE(2)) and intestinal hormones (CCK, gastrin, vasoactive intestinal polypeptide, secretin) also stimulated glandular secretion, whereas activation of submucosal secretomotor neurons by 5-hydroxytryptamine did not. This study directly demonstrates that multiple hormonal, inflammatory, and neurocrine agents activate Brunner's glands, whereas many have dissimilar effects on the epithelium. This suggests that Brunner's glands are regulated by pathways that act both in parallel to and in isolation from those controlling epithelial secretion.

Animals↗
PubMed2000

Dynamic regulation of mucus gel thickness in rat duodenum.

We examined the dynamic regulation of mucus gel thickness (MGT) in vivo in rat duodenum in response to luminal acid, cyclooxygenase (COX) inhibition, and exogenous PGE(2). An in vivo microscopic technique was used to measure MGT with fluorescent microspheres in urethan-anesthetized rats. Duodenal mucosa was topically superfused with pH 7.0 or pH 2.2 solutions with or without PGE(2) and indomethacin treatments. Glycoprotein concentration of duodenal loop perfusates was measured with periodic acid/Schiff (PAS) or Alcian blue (AB) staining. MGT and perfusate glycoprotein concentration were stable during a 35-min perfusion with pH 7.0 solution. Acid exposure increased MGT and PAS- and AB-positive perfusate glycoprotein concentrations. Indomethacin pretreatment increased both PAS- and AB-positive perfusate glycoprotein at baseline; subsequent acid superfusion decreased perfusate glycoproteins and gel thickness. PGE(2) (1 mg/kg iv) simultaneously increased MGT and PAS-positive perfusate glycoprotein concentrations followed by a transient increase in AB-positive glycoprotein concentration, suggesting contributions from goblet cells and Brunner's glands. Parallel changes in MGT and perfusate glycoprotein concentration in response to luminal acid and PGE(2) suggest that rapid MGT variations reflect alterations in the balance between mucus secretion and exudation, which in turn are regulated by a COX-related pathway. Luminal acid and PGE(2) augment mucus secretion from goblet cells and Brunner's glands.

Acids↗
PubMed2000

A duodenum-specific enhancer regulates expression along three axes in the small intestine.

Adenosine deaminase (ADA) is expressed at high levels in the epithelium of proximal small intestine. Transgenic mice were used to characterize the regulatory region governing this activation. A duodenum-specific enhancer is located in intron 2 of the human ADA gene at the central site among a cluster of seven DNase I-hypersensitive sites present in duodenal DNA. Flanking DNA, including the remaining hypersensitive sites, is required for consistent high-level enhancer function. The enhancer activates expression in a pattern identical to endogenous ADA along both the anterior-posterior axis of the small intestine and the crypt-villus differentiation axis of the intestinal epithelium. Timing of activation by the central enhancer mimics endogenous mouse ADA activation, occurring at 2-3 wk of age. However, two upstream DNA segments, one proximal and one distal, collaborate to change enhancer activation to a perinatal time point. Studies with duodenal nuclear extracts identified five distinct DNase I footprints within the enhancer. Protected regions encompass six putative binding sites for the transcription factor PDX-1, as well as proposed CDX, hepatocyte nuclear factor-4, and GATA-type sites.

Adenosine Deaminase↗
PubMed2000

Neural pathways regulating Brunner's gland secretion in guinea pig duodenum in vitro.

This study examined the neural pathways innervating Brunner's glands using a novel in vitro model of acinar secretion from Brunner's glands in submucosal preparations from the guinea pig duodenum. Neural pathways were activated by focal electrical stimulation and excitatory agonists, and videomicroscopy was used to monitor dilation of acinar lumen. Electrical stimulation of perivascular nerves evoked large dilations that were blocked by TTX (1 microM) or the muscarinic receptor antagonist 4-diphenylacetoxy-N-(2-chloroethyl)-piperidine hydrochloride (1 microM). The nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium iodide (100 microM) had no effect, and the nerve-evoked responses were not inhibited by hexamethonium (200 microM). Dilations were abolished in preparations from chronically vagotomized animals. Activation of submucosal ganglia significantly dilated submucosal arterioles but not Brunner's glands. Effects of electrical stimulation of perivascular and submucosal nerves were not altered by guanethidine. Capsaicin and substance P also dilated arterioles but had no effect on Brunner's glands. Cholinergic (choline acetyltransferase-immunoreactive) nerve fibers were found in Brunner's glands. These findings demonstrate that Brunner's glands are innervated by cholinergic vagal fibers but not by capsaicin-sensitive or intrinsic enteric nerves.

Animals↗
PubMed2001

COX inhibition excites enteric nerves that affect motility, alkaline secretion, and permeability in rat duodenum.

In anesthetized rats, the cyclooxygenase (COX) inhibitor indomethacin induces duodenal motility, increases duodenal mucosal alkaline secretion (DMAS), and evokes a transient increase in duodenal paracellular permeability (DPP). To examine whether enteric nerves influence these responses, the duodenum was perfused with lidocaine. Motility was assessed by measuring intraluminal pressure, and DPP was determined as blood-to-lumen clearance of (51)Cr-EDTA. DMAS was assessed by titration. In control animals, few contractions occurred during saline perfusion and lidocaine did not alter this condition. Perfusion with 0.03-0.1% lidocaine did not affect DMAS or DPP whereas 0.3-1% lidocaine reduced DMAS and increased DPP. Indomethacin induced motility and doubled DMAS. Application of 0.03% lidocaine on the duodenal serosa reduced motility and DMAS whereas 0.03% lidocaine applied luminally inhibited DMAS only. Higher concentrations of lidocaine abolished the increase in DMAS and changed the motility pattern to numerous low-amplitude contractions, the latter effect being blocked by iloprost. The lidocaine-induced increases in DPP were markedly higher than in controls. We conclude that indomethacin activates enteric nerves that induce motility, increase DMAS, and decrease DPP.

Alkalies↗
PubMed1976

Intestinal calcium absorption: differences in transport between duodenum and ileum.

The interaction of calcium with sugar, sodium, and water absorption was studied in rats fed laboratory chow and in vitamin D-deficient and -repleted rats with the use of intestinal loops in vivo. Calcium absorption in the duodenum was enhanced by D-glucose only in the vitamin D-deficient state. In both vitamin D-deficient and -repleted ileum, calcium absorption decreased when NaCl was replaced by mannitol; however, it remained unchanged when NaCl was replaced by choline chloride or urea. Calcium absorption was enhanced by actively transported sugars and by increasing net water flow generated by differences in osmotic pressure and urea. Under all experimental conditions there was a strong association between net water and calcium absorption in the ileum. These findings suggest that calcium absorption is enhanced by solvent drag, although the role of sodium cannot be excluded entirely.

Animals↗
PubMed2002

Phosphate transport in the duodenum and jejunum of goats and its adaptation by dietary phosphate and calcium.

Endogenous P(i) recycling is a characteristic feature of the P homeostasis in ruminants. A pronounced salivary P(i) secretion into the rumen is balanced by a high intestinal P(i) absorption and an almost complete renal P(i) reabsorption. In monogastric animals, the major P(i) transport mechanism across the apical membrane of the enterocyte is an Na(+)-dependent transport mediated by NaPi cotransporter type IIb. In ruminants, an Na(+)-, as well as an H(+)-dependent, P(i) transport system seems to exist in the small intestines. Therefore, morphological localization, type of ionic dependence, and ability to adapt to dietary P or Ca restriction of duodenal and jejunal P(i) transport were characterized in goats. In the duodenum, there was an H(+)-dependent, Na(+)-sensitive P(i) transport system that did not belong to the NaPi type II family and was not influenced by dietary P or Ca restriction. In contrast, in the jejunum, there was an Na(+)-dependent, H(+)-sensitive P(i) transport mainly mediated by NaPi IIb. P restriction stimulated the NaPi IIb protein expression, resulting in higher P(i) transport capacity.

Adaptation, Physiological↗
PubMed1986

Inhibition of Ca absorptive flux by chlorthalidone in the rat duodenum and colon.

To evaluate the mode and intestinal sites of action of chlorthalidone on Ca transport, balance and flux studies by the Ussing technique were performed in rats fed a low Ca diet throughout the experiment to stimulate Ca absorption. Half of the rats received chlorthalidone (5 mg X kg-1 X day-1) orally for 18 wk, a duration of administration previously shown to yield consistent changes. Net Ca absorption was decreased by chlorthalidone (0.91 +/- 0.07 vs. 1.08 +/- 0.3 mg/day, P less than 0.05), which is similar to prior observations in rats fed a normal Ca diet. Ca balance was unchanged by chlorthalidone (0.34 +/- 0.08 vs. 0.36 +/- 0.05 mg/day) because of concomitant hypocalciuria of similar magnitudes. In the duodenum, chlorthalidone decreased mucosal-to-serosal flux (Jm----s) (96.7 vs. 111.5 nmol X cm-2 X h-1, P less than 0.05). Since serosal-to-mucosal flux (Js----m) was unchanged, net Ca flux (Jnet) was reduced (74.0 vs. 89.6 nmol X cm-2 X h-1, P less than 0.05). Similarly, chlorthalidone selectively inhibited Jm----s in the descending colon (27.0 vs. 36.2 nmol X cm-2 X h-1, P less than 0.01), reducing Jnet (14.3 vs. 23.2 nmol X cm-2 X h-1, P less than 0.005). Short-circuit current and tissue conductance were unaffected. These data suggest that chronic chlorthalidone treatment reduces Ca absorption by inhibiting active calcium transport in the small and large intestine.

Absorption↗
PubMed1986

Ca fluxes across duodenum and colon of spontaneously hypertensive rats: effect of 1,25(OH)2D3.

Calcium absorption by spontaneously hypertensive rats (SHR) was variably reported to be different from normotensive Wistar-Kyoto (WKY) controls. Furthermore, blunted responsiveness to the intestinal effects of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] has also been postulated. To evaluate this hypothesis, calcium fluxes were measured by the Ussing technique across duodenum and descending colon with or without prior 1,25(OH)2D3 treatment. Duodenal mucosal-to-serosal calcium flux (Jm----s) (44.9 vs. 52.4 nmol X cm-2 X h-1), serosal-to-mucosal flux (Js----m) (25.6 vs. 28.4 nmol X cm-2 X h-1), and net flux (Jnet) were comparable. 1,25(OH)2D3 increased duodenal Jm----s in both SHR and WKY groups (95.2 and 86.8 nmol X cm-2 X h-1). Js----m was lower in SHR (26.1 vs. 35.6 nmol X cm-2 X h-1, P less than 0.01), although the tendency for a higher Jnet in SHR (68.6 vs. 51.2 nmoles X cm-2 X h-1) was statistically insignificant. Short-circuit current was higher in the colon of SHR, both before and after 1,25(OH)2D3, suggesting increased sodium transport. Basal colonic Jnet was virtually zero in both groups but comparably increased by 1,25(OH)2D3 because of stimulation in only Jm----s. Prevention of hypertension by hydralazine since the 4th wk of age did not alter the findings compared with the hypertensive SHR, suggesting calcium transport rates were unaffected by hypertension. These data indicate that in vitro, duodenal, and colonic active calcium transport by the SHR is similar to WKY. Their normal responses to 1,25(OH)2D3 do not support the hypothesis of intestinal resistance.

Animals↗
PubMed2001

Afterhyperpolarization current in myenteric neurons of the guinea pig duodenum.

Whole cell patch and cell-attached recordings were obtained from neurons in intact ganglia of the myenteric plexus of the guinea pig duodenum. Two classes of neuron were identified electrophysiologically: phasically firing AH neurons that had a pronounced slow afterhyperpolarization (AHP) and tonically firing S neurons that lacked a slow AHP. We investigated the properties of the slow AHP and the underlying current (I(AHP)) to address the roles of Ca(2+) entry and Ca(2+) release in the AHP and the characteristics of the K(+) channels that are activated. AH neurons had a resting potential of -54 mV and the AHP, which followed a volley of three suprathreshold depolarizing current pulses delivered at 50 Hz through the pipette, averaged 11 mV at its peak, which occurred 0.5-1 s following the stimulus. The duration of these AHPs averaged 7 s. Under voltage-clamp conditions, I(AHP)'s were recorded at holding potentials of -50 to -65 mV, following brief depolarization of AH neurons (20-100 ms) to positive potentials (+35 to +50 mV). The null potential of the I(AHP) at its peak was -89 mV. The AHP and I(AHP) were largely blocked by omega-conotoxin GVIA (0.6-1 microM). Both events were markedly decreased by caffeine (2-5 mM) and by ryanodine (10-20 microM) added to the bathing solution. Pharmacological suppression of the I(AHP) with TEA (20 mM) or charybdotoxin (50-100 nM) unmasked an early transient inward current at -55 mV following step depolarization that reversed at -34 mV and was inhibited by niflumic acid (50-100 microM). Mean-variance analysis performed on the decay of the I(AHP) revealed that the AHP K(+) channels have a mean chord conductance of ~10 pS, and there are ~4,000 per AH neuron. Spectral analysis showed that the AHP channels have a mean open dwell time of 2.8 ms. Cell-attached patch recordings from AH neurons confirmed that the channels that open following action currents have a small unitary conductance (10-17 pS) and open with a high probability (</=0.5) within the first 2 s following an action potential. These results indicate that the AHP is largely a consequence of Ca(2+) entry through omega-conotoxin GVIA-sensitive Ca(2+) channels during the action potential, Ca(2+)-triggered Ca(2+) release from caffeine-sensitive stores and the opening of Ca(2+)-sensitive small-conductance K(+) channels.

Action Potentials↗
PubMed2000

Nonceliac diaphragm disease of the duodenum.

A 58-year-old, Indo-Canadian man presented with upper abdominal pain and the clinical features of a partial, gastric outlet obstruction. Subsequent studies, including endoscopic examination, revealed diaphragm-like strictures in the descending duodenum. Other reported causes such as celiac disease and drug-induced small bowel diaphragms were excluded. Possibly, the changes seen in this patient were related to ethnic food-induced, mucosal injury to the upper gastrointestinal tract. Further studies are needed to evaluate potential toxicity or protective effects of different ethnic diets and their relationship with the development of different intestinal diseases.

Constriction, Pathologic↗
PubMed2005

Detection of a tyrosine phosphatase LAR on intestinal epithelial cells and intraepithelial lymphocytes in the human duodenum.

Studies of tyrosine phosphorylation in the human duodenum have indicated that proliferating cells in the middle portion of the duodenal crypt were devoid of this feature, suggesting that tyrosine kinase activation is not a dominant factor in crypt cell proliferation, and that consequently tyrosine phosphatase activity may be a more critical factor in crypt cell development. We investigated the expression of the leukocyte common antigen-related receptor (LAR) family of tyrosine phosphatases. A flow cytometry system was used to examine cells from the surface, mid-portion, and lower part of the crypt. Individual cell populations were immunostained with anti-LAR antibodies using phycoerythrin-conjugated anti-CD3 to discriminate between epithelial cells (CD3-) and intraepithelial lymphocytes (CD3+). Epithelial cells expressed LAR throughout the crypt. Expression of LAR was maximal in the mid-portion of the crypt with lower expression at the top of the villi. Intraepithelial lymphocytes expressed low levels of LAR at the tips of the villi with stronger expression extending towards the base of the crypt. These findings were confirmed by immunohistochemistry on paraffin-fixed sections. Of note, peripheral blood lymphocytes expressed less LAR than IEL. These observations suggest the possibility that tyrosine phosphatase LAR may be of importance in the regulation of crypt cell proliferation. Moreover, as the extracellular domain of LAR has homology with adhesion molecules, the finding of this molecule on IEL could suggest a possible functional role in homing of this unique lymphocyte.

CD3 Complex↗
PubMed1999

Junctional transmissions in smooth muscle of the guinea pig duodenum and their modulation by the prokinetic agent DQ-2511.

Junctional transmissions and their modulation by DQ-2511, a novel prokinetic agent, were investigated in smooth muscle of the guinea pig duodenum. Transmural nerve stimulation evoked a cholinergic excitatory junction potential, a nonadrenergic, noncholinergic inhibitory junction potential, and a substance P mediated slow depolarization. DQ-2511 showed dual effects on the slow depolarization: a low concentration (10(-9) mol/l) enhanced and high concentrations (>10(-6) mol/l) tended to inhibit. The depolarization produced by exogenously applied substance P was enhanced by low concentrations of DQ-2511. The results suggest that the prokinetic actions of DQ-2511 involve an enhancement of transmission from substance P neurons due to an increase in sensitivity of postjunctional receptors to substance P.

Analgesics↗