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PubMed1990

Influence of Cl- on pH(i) in oxynticopeptic cells of in vitro frog gastric mucosa.

The effect of Cl- on intracellular pH (pH(i)) was studied using sheets of frog (Rana catesbeiana) fundic mucosa in which oxynticopeptic cells were selectively loaded with the acetomethoxy ester form of the pH-sensitive fluorescent dye 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF/AM). Before the measurement of pH(i), tissues were exposed to either 10(-5) M forskolin in the serosal solution (stimulated tissues) or 3 x 10(-4) omeprazole in the serosal solution (inhibited tissues). In HCO3- and N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) buffers, pH(i) increased significantly after removal of Cl- from serosal and luminal solution, both in stimulated and inhibited tissues. The presence of Cl- in the luminal solution prevented this rise in pHi, an effect abolished by serosal 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS, 3 x 10(-4) M) but not by serosal amiloride (10(-3)M). In the presence of serosal Cl-, pH(i) increased after exposure to serosal DIDS, more prominently in the stimulated than in the inhibited tissues. These results confirm the presence of a Cl(-)-HCO3-exchanger in the basolateral membrane of oxynticopeptic cells in intact sheets of mucosa and suggest that luminal Cl- contributes to the regulation of pH(i) in oxynticopeptic cells.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1975

Ileal HCO3 secretion: relationship to Na and Cl transport and effect of theophylline.

Interrelationships among Na, Cl, and HCO3 transport processes were examined in short-circuited rabbit ileal mucosa. As serosal (HCO3) was increased from 10 to 50 mM (pH from 7.1 to 7.8), net Na absorption decreased from 4.6 to 0.3 mueq/h-cm2, net Cl flux changed from absorption of 0.9 to secretion of 0.9 and a net HCO3 secretion of 3.0 developed. A similar change in net Cl flux was also observed when serosal Pco2 was altered at constant (HCO3). In Cl-free SO4-Ringer, serosal alkalinization produced net HCO3 secretion which was not significantly less than that observed in Cl-containing Ringer. Theophylline caused secretory changes in net Na and Cl fluxes at both 10 and 50 mM serosal (HCO3). Theophylline did not alter net HCO3 flux in Cl-Ringer but increased net HCO3 flux in SO4-Ringer. Total dc conductance was decreased by both serosal alkalinization and theophylline. Shortcircuit current was consistently increased by theophylline but not by serosal alkalinization. The results indicate that ileal ion transport is regulated in part by serosal pH and/or (HCO3) and that resulting changes in Cl and HCO3 transport are coupled one-for-one with changes in Na transport. Furthermore, HCO3 secretion does not require the presence of Cl in the bathing medium.

Animals↗
PubMed2006

Kinetics of urothelial ATP release.

Recent reports have proposed that the urothelium can sense mechanical stretch and communicate this information to sensory afferent neurons by the release of ATP into the vicinity of P2X-containing neurons. This report investigates the bidirectional release of ATP by in vitro rabbit urothelium. ATP was measured using the luciferin-luciferase assay. Immediately after washing of both sides of the epithelium, there was a linear increase in ATP content in the mucosal compartment with a rate of 23 +/- 6.5 fmol x min(-1) x cm(-2) (n = 18). Serosal ATP content increased as a saturating exponential function, suggesting a constant rate of release and degradation of ATP by ectonucleotidases/exonucleotidases. The presence of a serosal ectonucleotidase/exonucleotidases was demonstrated by the time-dependent decrease in exogenously added ATP. The maximum rate of hydrolysis was 11 pmol x min(-1) x cm(-2) with a K(m) of 0.49 microM. The time course of serosal ATP release was modeled as a constant rate of release (d: mol x min(-1) x cm(-2)) and rate constant of hydrolysis (k(h): min(-)). In control conditions d was 18 fmol x min(-1) x cm(-2) and k(h) of 0.056 +/- 0.01 min(-) (n = 18). Steady-state serosal chamber content is 370 +/- 90 fmol/cm(2), and concentration is 50 +/- 1.2 x 10(-12) M. Stretching the tissue resulted in a transient fivefold increase in the rate of mucosal ATP release and a transient sixfold increase in serosal ATP release. Half-osmotic strength solutions increased mucosal release by 10-fold and serosal release by 5-fold. Tissue damage resulted in a step-increase in mucosal chamber ATP content by 6.6 +/- 1 pmol/cm(2) and serosal chamber ATP by 0.1 +/- 0.06 pmol/cm(2) (n = 5).

Adenosine Triphosphate↗
PubMed1994

Role of intracellular Ca2+ in modulation of tight junction resistance in A6 cells.

The role of intracellular Ca2+ in the development and maintenance of epithelial tight junctional integrity is poorly understood. We assessed tight junctional resistance (Rj) in confluent monolayers of A6 cells that were treated with mucosal amiloride such that the transepithelial resistance (Rt) reflects Rj. Solution Ca2+ concentration [Ca2+] was reduced by ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) addition to the bathing solutions. Reduction of mucosal [Ca2+] to 1 microM or reduction of serosal Ca2+ to 100 microM did not significantly alter Rt. However, a further decrease of serosal Ca2+ to 40 microM caused the resistance to fall to < 12% of the control value. Following restoration of serosal [Ca2+], Rt increased to a new steady-state value within approximately 15 min. The magnitude of recovery of Rt was inversely correlated with the length of time the epithelium was exposed to low serosal [Ca2+]. To further test the effects of asymmetric Ca2+ removal, the serosal [Ca2+] was chelated using EGTA to reduce Rt. When the Ca2+ ionophore A-23187 was subsequently added to the mucosal solution, Rt increased from 20% to 60% of the control level. In addition, cells were loaded with the fluorescent Ca2+ indicator, Calcium Green, and the temporal relationship between changes in Rt and intracellular Ca2+ was determined. Following removal of serosal Ca2+, cell Ca2+ decreased, followed by a decrease in Rt. In contrast, returning Ca2+ to the serosal bathing solution resulted in a parallel increase of both Rt and cell [Ca2+]. These data strongly suggest that changes in intracellular [Ca2+] play an important role in the regulation of Rj.

Amiloride↗
PubMed1978

Inhibition of the bicarbonate exit step in urinary acidification by a disulfonic stilbene.

Acidification of the luminal solution by the isolated turtle bladder involves H(+) secretion by a pump at the luminal membrane. The OH(-) dissociated in this process reacts with CO(2) and forms HCO(3) (-) which moves passively out of the cell across the serosal cell membrane. In the present study, this exit step for HCO(3) (-) was inhibited by serosal addition of the disulfonic stilbene, SITS, an agent which is thought to bind to a transport protein at the serosal cell membrane. 90 min after serosal addition of 0.5 mM SITS, H(+) secretion decreased by > 80%. In contrast, luminal addition of SITS had no effect. During inhibition of H(+) secretion by serosal SITS, overall cell pH, measured by the 5, 5-dimethyl-2, 3-oxazolidinedione method, increased from 7.48+/-0.03 to 7.61+/-0.02. This increase of 0.13+/-0.02 pH U was associated with a much larger regional pH increase as judged from the decrement in the attainable pH gradient across the epithelium. After serosal SITS, this gradient was reduced from 2.88+/-0.06 to 2.09+/-0.11 pH U. In the absence of evidence for increased H(+) permeability or a change in the force of the H(+) pump, the gradient decrement of 0.79+/-0.08 U reflects a similar pH increment on the cytoplasmic side of the pump.SITS inhibits the exit of bicarbonate across the serosal cell membrane and, thereby, creates a compartment of high alkalinity in series with the pump. The increased electrochemical gradient across the active transport pathway is the primary factor in the inhibition of urinary acidification.

Acid-Base Equilibrium↗
PubMed2000

Stimulation of Cl(-) secretion by L-alanine oligopeptides in the mammalian large intestine.

A variety of oligopeptides are probably released within the intestinal tissue under inflammatory conditions or during peptide absorption. To examine whether some of these peptides can affect intestinal transport functions, we determined the effects of L-alanine oligopeptide on short-circuit current (I(sc)) and transmucosal conductance (G(t)) in submucosa-mucosa preparations from the mouse cecum and guinea pig distal colon in vitro in Ussing chambers. L-Alanyl-L-alanine (Ala-Ala, 10 mM) added to the serosal side increased I(sc) and G(t), giving a peak followed by a sustained phase (the peak increase in I(sc) was 45 +/-6 microA/cm(2) and the increase in G(t) was 0.55+/-0.11 mS/cm(2)). The tripeptide, L-alanyl-L-alanyl-L-alanine (Ala-Ala-Ala, 10 mM), added to the serosal side also induced increases in I(sc) and G(t) by a similar degree. On the other hand, luminal Ala-Ala, and serosal L-alanine and L-alanine (10 mM) caused significantly smaller increases in I(sc) and G(t) ( approximately 15 microA/cm(2) and approximately 0. 15 mS/cm(2), respectively). The Ala-Ala induced increase in I(sc) was partially inhibited by serosal bumetanide (0.1 mM) and mucosal 5-nitro-2-(3-phenylpropylamino)benzoic acid (0.1 mM), and largely suppressed by removing Cl(-) from the bathing solution. The increase in I(sc) was largely suppressed by serosal low Ca(2+) and tetrodotoxin, but was not affected by indomethacin. In the guinea pig distal colon, serosal Ala-Ala (10 mM) evoked a transient increase in I(sc) by 23+/-7 microA/cm(2) and an increase in G(t) by 1.2+/-0.3 mS/cm(2). These results suggest that Ala-Ala, and probably also Ala-Ala-Ala, added to the serosal side stimulated electrogenic Cl(-) secretion mainly through the activation of submucosal secretomotor neurons in the mammalian large intestine.

Alanine↗
PubMed2000

Urea modifies the permeability of the mammalian urothelium.

PURPOSE: This study investigated the effects of mucosal (urine side) and serosal (blood side) urea on the permeability properties of the in vitro mammalian urinary bladder epithelium. MATERIALS AND METHODS: The permeability properties of the rabbit urinary bladder epithelium were studied in modified Ussing chambers using electrophysiological techniques. RESULTS: Addition of two molar urea to the mucosal solution did not cause a significant change in the short circuit current (Isc, a measure of the ion transport capacity of the epithelium), or the transepithelial conductance (Gt, a measure of the ability of ions to diffuse across the epithelium). In contrast, addition of 0.5 M urea to the serosal solution caused an increase in Gt of approximately 35 microS/cm.2 as well as an increase in Isc over a 5 minute period. The site of the conductance increase by short-term serosal urea was at the apical membrane and not at the tight junctions. The urea-induced conductance completely reversed upon removal of urea, was non-selective, and the magnitude was voltage dependent. Long term serosal urea (greater than 30 minutes) resulted in an irreversible increase in transepithelial conductance. Mucosal urea altered the time course but not the magnitude of the serosal urea-induced conductance. CONCLUSIONS: The ion permeability of the mammalian urinary bladder is increased by serosal urea. At short times the increase is at the apical membrane, while at long times the increase is at the tight junctions. The presence of mucosal urea slows the loss of urothelial barrier function caused by serosal urea.

Animals↗
PubMed2003

Indications for a pylorus-preserving gastrectomy for gastric cancer with proper muscle invasion.

HYPOTHESIS: Our previous demonstrations of the feasibility of a pylorus-preserving gastrectomy with a wider-scope lymphadenectomy for early gastric cancer (GC) have raised the possibility of applying pylorus-preserving gastrectomy to a broader segment of GC patients, such as those having GC with invasion extending into the proper muscle layer (GCpm). DESIGN: Case series. SETTING: Tertiary care center. PATIENTS: This study comprised 107 patients with solitary primary GCpm located in the middle or lower third of the stomach. INTERVENTION: All patients underwent gastrectomy, using at least the former D2 dissection of the American Joint Committee on Cancer. MAIN OUTCOME MEASURES: Patterns and sites of nodal involvement were analyzed in relationship to other clinicopathologic characteristics, including preoperative and intraoperative evaluations of tumor depth (cT), nodal involvement (cN), and serosal involvement. The conditions required were serosal negativity and measurements less than or equal to cT2 cN0 with histologic proof of node negativity, or if positive, the positive nodes had to be confined to the first or selective second tier. The selective second-tier nodes were defined as those along the left gastric, common hepatic, and celiac arteries. RESULTS: The factors favoring node negativity were serosal negativity, cN0, or both. For tumors that were serosal-negative and less than or equal to cT2 cN0 to meet the above conditions, a tumor in the middle third of the stomach had to be less than or equal to 2 cm in the maximum diameter, and that in the lower third could be any size. No patients with serosal negativity and cT2 cN0 GCpm less than or equal to 2 cm in diameter died of cancer or had positive nodes beyond the selective second tier. CONCLUSIONS: Considering the required distance between the pyloric ring and distal margin of the tumor to avoid a positive resection margin, pylorus-preserving gastrectomy with a selective second-tier node dissection is optimal for tumors that are serosal negative, less than or equal to cT2 cN0, and less than or equal to 2 cm in maximum diameter when located in the middle or lower third of the stomach.

Aged↗
PubMed1995

Transmural gut oxygen gradients in shocked rats resuscitated with heparan.

OBJECTIVES: To develop a reproducible model to measure transmural gut tissue PO2, to determine the gradient from serosa to mucosa during normovolemia and hypovolemia, and to determine the effect of resuscitation with heparan sulfate (danaparoid sodium) on this gradient. DESIGN: Fluorescent tissue oxygen sensors were placed onto serosal and mucosal surfaces of rat colon. Hemorrhagic shock was induced using a fixed pressure (mean arterial pressure, 40 mm Hg) model and resuscitated with either saline solution or heparan. RESULTS: Control animals had stable mean (+/- SD) serosal and mucosal tissue oxygen tensions (PO2) of 64 +/- 4 and 10 +/- 2 mm Hg, respectively. In shocked animals, baseline serosal PO2 decreased to 37 +/- 2 mm Hg at a mean (+/- SD) of 19 +/- 7 minutes after the initiation of hemorrhage. Mucosal values decreased to a minimum of 4 +/- 2 mm Hg at 45 +/- 15 minutes after the initiation of hemorrhage. Serosal PO2 returned to baseline during resuscitation in both control and heparan-resuscitated animals. Mucosal PO2 did not return to baseline in the shock/no heparan group. In the heparan-resuscitated animals, however, mucosal PO2 increased above baseline (13 +/- 3 mm Hg at 3 hours after completion of hemorrhage). CONCLUSIONS: A transmural gradient of PO2 exists across the colon with mucosal PO2 far lower than serosal PO2. Both serosal and mucosal PO2 decrease during hypovolemia. During hypovolemia, the PO2 of the entire gut wall is in a range in which phagocytic killing is impaired by hypoxia. Heparan improved mucosal PO2 and it may restore and/or protect gut function by oxygen-related mechanisms.

Analysis of Variance↗
PubMed1990

System approach to the transepithelial transport across rat jejunal enterocytes: effect of cytochalasin B, colchicine, and ethylenediaminetetraacetic acid on butyric acid transport.

A three-compartment physical model is devised for transepithelial passive transport across intestinal cells. The mathematical equations derived from the model allow the simultaneous and quantitative measurements, in the form of permeability coefficients, of solute transport across both the luminal-serosal and serosal-blood barriers. The proposed model is used to study the involvement of the cytoskeleton in butyric acid absorption by the rat jejunum. Alterations in cytoskeletal functions are introduced by the administration of microfilamentous and microtubular altering agents such as cytochalasin, colchicine, or EDTA. An isolated jejunal segment perfused with a buffer containing labeled butyric acid was homogenized at the end of the experiment and assayed for its butyric acid content. During the perfusion, portal blood samples, as well as perfusate samples collected 10 cm distal to the perfusion site were drawn at 5-min intervals and assayed for their radioactivity. Cytochalasin was found to decrease the permeability of the mucosal membrane to butyric acid and to increase that of the serosal membrane. Colchicine did not have any effect either on the mucosal or on the serosal side. Cytochalasin and colchicine, when given in the same experiment, increased the permeability of the serosal membrane to butyric acid, but were without any effect on the mucosal barrier. Also, EDTA had no effect on the mucosal side, but decreased significantly the permeability of the serosal membrane to the fatty acid.

Animals↗
PubMed1994

Model of bicarbonate secretion by resting frog stomach fundus mucosa. I. Transepithelial measurements.

In the present in vitro experiments on gastric fundus mucosa of Rana esculenta we try to define the mechanism of alkaline secretion that is observed in summer frogs in the resting stomach (blockage of HCl secretion by ranitidine, 10(-5) mol/l). The transepithelial voltage and the rate of alkalinization (ASR) of an unbuffered gastric lumen perfusate was measured as a function of serosal (and mucosal) fluid composition. ASR was high (0.88 +/- S.E. 0.09 microEq.cm-2.h-1, n = 11) during serosal bath perfusion with HCO(3-)-Ringer solution, decreased slightly to 0.50 +/- 0.07 microEq.cm-2.h-1 (n = 6) in HCO(3-)-free HEPES-buffered Ringer solution of the same pH, and decreased to approximately 20% when carbonic anhydrase was inhibited by acetazolamide. While replacement of mucosal or serosal Cl- did not--within 1 h--significantly alter ASR, replacement of serosal Na+ in the presence or absence of HCO3- strongly reduced ASR, and a similar reduction was observed after serosal application of the anion transport inhibitor DIDS (4,4-diisothiocyanatostilbene-2,2-disulphonate, 2.10(-4) mol/l), the metabolic poison rotenone (10(-5) mol/l), the uncoupler dinitrophenol (10(-4) mol/l), and the Na+ pump inhibitor ouabain (10(-4) mol/l), while serosal amiloride (10(-4) mol/l) had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1990

Transcellular bicarbonate transport in rabbit gallbladder epithelium: mechanisms and effects of cyclic AMP.

HCO3 permeation through rabbit gallbladder epithelium has been investigated in vitro using voltage-clamp, pH-stat and microelectrode techniques. Mucosa-to-serosa flux of HCO3 (approximately 4.9 mumol cm-2 h-1) was dependent on luminal Na and inhibited by amiloride (1 mmol/l, luminal bath), methazolamide (0.1 mmol/l, both sides), and ouabain (30 mumol/l, serosal bath). Maximal rates of serosa-to-mucosa flux of HCO3 (approximately 2.8 mumol cm-2 h-1) required serosal Na and mucosal Cl. This flux was inhibited by ouabain, 4-acetamido-4'-isothiocyanato-stilbene-2,2'-disulfonic acid (1 mmol/l, serosal bath), and 5-nitro-2-(3-phenylpropylamino)-benzoic acid (0.1 mmol/l, luminal bath). Ineffective were methazolamide (0.1 mmol/l, both sides) and amiloride (1 mmol/l, serosal bath). 8-Br-cAMP (1 mmol/l, serosal bath) largely inhibited the absorptive and moderately stimulated the secretory flux. In tissue conductance, short-circuit current, and transmural voltage prostaglandin E1 (1 mumol/l, serosal bath) and 8-Br-cAMP caused moderate to negligible increases. No significant alterations of apical membrane potential (approximately -65 mV) and the apparent ratio of membrane resistances (Ra/Rb; approximately 1.9) were found. Cell membranes responded to luminal Cl removal mostly with a slow hyperpolarization that was mitigated by 8-Br-cAMP or, in some cases, converted into a small, transient depolarization. Our results are best explained by transcellular HCO3 transport in both directions. In secretion, basolateral HCO3 entry occurs by some form of co-transport with Na, and apical exit by Cl/HCO3 exchange. cAMP opens no major electro-diffusive pathway for apical anion efflux. In absorption, HCO3 import from the lumen into the cell is secondary to cAMP-sensitive Na/H exchange.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1982

Effect of hydrostatic pressure on ADH induced osmotic water flow in toad bladder.

The effect of hydrostatic pressure (HP) on antidiuretic hormone (ADH) stimulated osmotic water flow (Jv) across the toad urinary bladder was evaluated. Jv for ADH-stimulated bladders was significantly reduced by an elevation of the serosal HP gradient to 1 cm H2O. Subsequent elimination of the HP gradient resulted in a recovery of Jv. Serosal HP also caused a reversible increase in sucrose permeability (P sucrose). For ADH-treated bladders fixed with glutaraldehyde during serosal HP exposure, subsequent exposure to a mucosal or serosal HP gradient caused acceleration or inhibition of Jv, respectively. The reduction in ADH-associated Jv with serosal HP was apparently caused by a back-flux of water through a paracellular pathway. Jv and P sucrose were not affected by mucosal HP during ADH stimulation. The results suggest a specific sensitivity of a paracellular pathway to a small serosal HP gradient in bladders with ADH-stimulated water flow. The reversibility of this effect on P sucrose suggests that the elements comprising the apical junctions are dynamic structures capable of recovering at least some of their permeability properties.

Animals↗
PubMed1982

The modulation by glucose transport of the electrical responses to hypertonic solutions of the goldfish intestinal epithelium.

Goldfish intestinal epithelium responds to mucosal hypertonicity with a negative biphasic transepithelial potential change and a relatively slow rise in transepithelial resistance, similar to that described for rabbit gallbladder (Wright et al. 1972; Smulders et al. 1972). In addition, the increase in resistance in goldfish intestine can be modulated by the presence or absence of glucose. E.g. during mucosal hypertonicity of 87 mosmoles/l the addition of 27.8 mmoles/l glucose to the serosal side further increased the resistance by 2.8 +/- 0.2 omega cm2, while mucosal addition reduced it by 11.2 +/- 2.6 omega cm2. Ouabain poisoning inverted this last response into a slowly and continuously rising resistance. The resistance response to mucosal glucose can be fully abolished by mucosal addition of phlorizin. The resistance change due to bilateral glucose addition is the sum of the separate mucosal and serosal responses. The effect of fructose at the serosal side resembles that of glucose added serosally; the mucosal effect of glucose could not be mimicked by fructose, but the decrease induced was of the same magnitude as the serosal effect of glucose, but of opposite sign. The effects of serosal addition of glucose and fructose and mucosal addition of fructose can be explained by different reflection coefficients of the cell membranes for glucose, fructose and mannitol. The mucosal effect of glucose is explained by a glucose-dependent influx of sodium at the mucosal side, stimulating a ouabain-sensitive pump at the baso-lateral aspects of the cell.

Animals↗
PubMed1979

Extracellular space determination in rat small intestine by using markers of different molecular weights.

The apparent extracellular space (ECS) of rat jejunum, everted and cannulated "in vitro", has been measured by using extracellular markers of different molecular weights. The markers used were two polyethyleneglycols, 14C and 3H labelled (14C-PEG MW 4000 and 3H-PEG MW 900) and 3H-sucrose. The ECSs for the mucosal and serosal sides have been separately determined throughout the time course, and it has been found that the two spaces are identical when PEG 4000 was used but the serosal ECS is almost the double when using PEG 900. The serosal ECS determined with sucrose is four times as big as the mucosal ECS. It seems reasonable to conclude that the best marker for the measure of total apparent ECS is sucrose, placed in the serosal compartment, taking into account that the mucosal ECS is four times smaller than the serosal one. All the markers used reach equilibrium with ECS, more rapidly in the mucosal than in the serosal ECS. Finally, by comparing cell water and cell Na concentrations, one observes that there is a statistical difference between the results obtained by using PEG 4000 as an extracellular marker and those obtained with sucrose.

Animals↗
PubMed1989

Unidirectional duodenal and jejunal calcium and phosphorus transport in the rat: effects of dietary phosphorus depletion, ethane-1-hydroxy-1,1-diphosphonate and 1,25 dihydroxycholecalciferol.

Unidirectional calcium (Ca) and phosphorus (Pi) transport was studied in vitro by means of a modified Using technique in the absence of electrochemical gradients between the mucosal and serosal buffer medium. Duodenum and jejunum of male albino Sprague-Dawley rats were investigated after Pi depletion alone (0.03% diet-Pi), Pi depletion and EHDP treatment (40 mg/kg per day s.c. X 4), and Pi depletion, EHDP and 1,25(OH)2D3 (500 pmol i.v. X 2) treatment. Mucosal-to-serosal Ca and Pi fluxes (Jms) changed in parallel, depending on the 1,25(OH)2D3-status of the animals. Regarding serosal-to-mucosal fluxes (Jsm), Pi depletion resulted in an increase in Jsm for Ca and Pi, associated with a rise in Gt and Isc in the duodenum but not in the jejunum. EHDP administered to block synthesis of 1,25(OH)2D3 caused further augmentation in duodenal Jsm for calcium but not phosphorus, which was paralleled by an increase in Gt and Isc. After repletion with 1,25(OH)2D3, an increase in Jsm for Ca and Pi and a rise in Gt and Isc were observed in the duodenum and in the jejunum. Serosal-to-mucosal fluxes for Ca and Pi were related to tissue conductance (Gt) in the duodenum (r = 0.89, P less than 0.001 and r = 0.84; P less than 0.001, respectively), as well as in the jejunum (r = 0.55; P less than 0.01 and r = 0.66; P less than 0.001, respectively). Changes in Jsm also paralleled changes in transmural shortcircuit current (Isc). The data are compatible with the assumption of an increase in Jsm for Ca and Pi and a rise in Gt, both reflecting an increase in water recycling across the tight junctions caused by a rise in sodium absorption. They provide further evidence that the overall effect of 1,25(OH)2D3 on intestinal Ca and Pi transport is to increase both cell-mediated active mucosal-to-serosal transport and paracellular diffusional serosal-to-mucosal ion movement.

Animals↗
PubMed1991

Mechanisms of acid injury to rabbit esophageal epithelium. Role of basolateral cell membrane acidification.

Because mucosal HCl traverses the paracellular pathway before significant damage develops within esophageal epithelium, the effects of mucosal and serosal acidification were compared on Ussing-chambered rabbit esophageal epithelia. Notably serosal, but not mucosal, acidification was associated with cell necrosis, and the latter was accompanied by abolition of potential difference and short-circuit current. The reason for this difference was explored by exposing tissues serosally to ouabain, chloride-free solution, 4-acetamido-4'-isothiocyanatostilbene-2-2'-disulfonic acid (SITS), or amiloride. The results show that serosal acidification, but not ouabainization, is associated with cell necrosis and that cell necrosis induced by serosal acidification can be blocked by SITS and chloride-free solution, but not by amiloride. These findings are compatible with the hypothesis that serosal acidification is more damaging than mucosal acidification because of the greater rate with which hydrogen ions can traverse the basolateral membrane; also, the route for more rapid entry appears to involve a SITS-sensitive, chloride-dependent mechanism (e.g., Cl/HCO3 antiport).

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1984

Absorption and metabolism of allopurinol and oxypurinol by rat jejunum in vitro: effects on uric acid transport.

The transport and metabolism of allopurinol and oxypurinol have been examined in a preparation of adult rat jejunum in vitro. When present in the lumen (50-500 mumol/l) allopurinol appeared in the serosal secretions at lower concentrations, together with its metabolite oxypurinol and an unidentified substance. Oxypurinol in the lumen (1.4-430 mumol/l) was transported into the serosal secretions and at luminal concentrations below approximately 150 mumol/l was concentrated in the secretions. The transport of oxypurinol into serosal secretions was greater than that of allopurinol. Allopurinol and oxypurinol decreased the appearance of urate, in the serosal secretions and the luminal fluid, by an amount which was greater than the concomitant increase in oxypurines; they increased the rate constant of the mono-exponential washout of endogenous urate and induced purine secretion into the lumen. The transport of uric acid from the lumen into the serosal secretions was inhibited by allopurinol and oxypurinol. With allopurinol the specific radioactivity (14C) of urate in the serosal secretions approached that in the lumen; with oxypurinol the specific radioactivity was approximately 70% that in the lumen. There was no evidence for the uphill movement of urate from the lumen.

Allopurinol↗