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At least 1,099 records · Page 61Linked to original sources
PubMed1989

Effects of 1,25(OH)2D3 on enterocyte basolateral membrane Ca transport in rats.

One, twenty-five dihydroxyvitamin D3 [1,25(OH)2D3], commonly known as calcitriol, stimulates intestinal Ca absorption through increased activity of a cellular transport process. To determine whether transcellular Ca transport involves energy-dependent Ca efflux across enterocyte plasma membrane in vitamin D-sufficient rats, in vitro bidirectional Ca fluxes were measured under short-circuited conditions across proximal duodenum from rats fed diets adequate in vitamin D and containing a normal Ca diet (NCD), a low Ca diet (LCD), or fed NCD and injected with 50 ng of 1,25(OH)2D3 daily for 4 days before study. LCD or 1,25(OH)2D3 increased Ca net flux [Jnet, mucosal-to-serosal flux minus the serosal-to-mucosal flux] by increasing Ca mucosal-to-serosal flux (Jm----s) (mean +/- SE, NCD vs. LCD vs. 1,25(OH)2D3, 16 +/- 4 vs. 179 +/- 18 vs. 82 +/- 21 nmol.cm-2. h-1, P less than 0.0001). Initial ATP-dependent Ca uptake rates by duodenal basolateral membrane vesicles (BLMV) was greater in vesicles from rats fed NCD compared with LCD and not different from NCD injected with 1,25(OH)2D3. These studies suggest that in vitamin D-replete animals, 1,25(OH)2D3 increases epithelial Ca Jm----s by mechanisms that do not involve ATP-dependent BLM Ca efflux. ATP-dependent Ca exit from the cell under these conditions may play a role in intracellular Ca homeostasis rather than Ca absorption.

Animals↗
PubMed1991

Characteristics of luminal bicarbonate secretion by rat cecum in vitro.

Under in vitro conditions the rat cecum transported HCO3- from the serosal to an unbuffered solution in contact with the mucosal side [Js----m = 7.12 +/- 0.18 mumol.cm-2.h-1 (n = 149)]. With reversed tissues, a significantly lower flux was obtained [Jm----s = 2.47 +/- 0.11 mumol.cm-2.h-1 (n = 42)]. Both fluxes were stable for several hours. Increasing the H+ gradient across the tissue for 60 min did not change either flux. Anoxia for 45 min reversibly reduced Js----m by 65 +/- 3% (n = 20) but had no effect on Jm----s. Both fluxes were linearly related to HCO3- concentration on the buffered side, but the slope for Js----m was 3.5 times that for Jm----s. When tissues were initially set up in HEPES buffer rather than HCO3-, Js----m was 0.12 +/- 0.05 mumol.cm-2.h-1 (n = 6), which is not significantly different from zero. Replacement of Na+ by choline reduced Js----m by 40 +/- 3% (n = 11) and ouabain (1 mM) by 24 +/- 3% (n = 5). Replacement of Cl- with isethionate or K+ with Na+ for 60 min did not alter Js----m. Serosal application of DIDS (0.5 mM) reduced Js----m by 24 +/- 6% (n = 6), but SITS (0.5 mM), furosemide (1 mM), acetazolamide (0.1 mM), amiloride (1 mM), and a proton pump inhibitor (Sch 28080, 50 microM) had no effect. Mucosal application of DIDS, furosemide, and amiloride had no effect on Js----m. Serosal tetrodotoxin (1 microM) and indomethacin (28 microM) were also without effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Avian cecum: role of glucose and volatile fatty acids in transepithelial ion transport.

In the fowl cecum in vitro, the influence of glucose and the three most prevalent naturally occurring volatile fatty acids (acetate, propionate, butyrate) on short-circuit current (Isc), electrical resistance, and transport of Na and Cl was determined. When glucose, acetate, or butyrate was present, ion transport was characterized by electrogenic Na absorption, greater than 65% of which was amiloride inhibitable, and Cl secretion, which also was electrogenic. Isc could be completely accounted for by net fluxes of Na and Cl. When glucose, acetate, or butyrate (10 mM both sides) was included in the incubation medium, cecal tissue maintained its Isc and a constant rate of net Na absorption and Cl secretion for a 5-h period. When no substrate was present or propionate was included in the medium, a marked fall in Isc and net Na and Cl fluxes was seen. Glucose caused an increase in Isc when added only to the serosal side. As 3-O-methylglucose (not metabolized) was not effective in stimulating Isc of the cecum (serosal or mucosal addition), it appeared that glucose increased Isc by acting as an energy substrate for active Na transport. Acetate and butyrate appeared to be equally effective in stimulating Na transport and Isc when placed on either side of the membrane. When the preparation was supplied with glucose (serosal side) and acetate was added to the mucosal side, no further stimulation of Isc occurred. Thus it appeared that acetate and butyrate were acting as substrates for active Na transport rather than stimulating Na transport by some other mechanism such as a cotransport with Na.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗
PubMed1992

Prostaglandin stimulates Cl(-)-HCO3- exchange in amphibian oxynticopeptic cells.

Prostaglandins, shown to stimulate Cl- transport in epithelial cells of several different tissues, protect gastric mucosa against physiological injury induced by luminal acid. To clarify the relationship between the stimulation of Cl(-)-transport and the protection of gastric mucosa, the effect of prostaglandin on Cl(-)-HCO3- exchange in oxynticopeptic cells (OPC) was examined in intact sheets of in vitro frog gastric mucosa, in which OPC were selectively loaded with the pH-sensitive fluorescent dye 2',7'-bis(carboxyethyl)-5(6')-carboxyfluorescein (BCECF). In omeprazole (0.3 mM)-pretreated frog fundic mucosae, in which H+ secretion was totally inhibited, 16,16-dimethyl prostaglandin E2 (dmPGE2) induced a significant decrease in intracellular pH (pHi) in OPC simultaneously with a significant increase in pHi in adjacent muscularis mucosae, an effect abolished by removal of ambient Cl- or addition of 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) (0.5 mM). dmPGE2 accentuated the rates of alkalinization of OPC after either removal of ambient Cl- or addition of serosal H2DIDS. During exposure to luminal or serosal acid, dmPGE2 significantly attenuated acidification of OPC induced by the exogenous H+, effects abolished either by removal of ambient Cl- or by addition of H2DIDS (0.5 mM). These results suggest that 1) dmPGE2 stimulates extrusion of HCO3- through the basolateral Cl(-)-HCO3- exchanger in resting OPC (H+ secretion inhibited) and that 2) relatively high extracellular [HCO3-] on the basolateral surface afforded by dmPGE2 protects OPC from acidification during exposure to luminal or serosal acid.

Animals↗
PubMed1992

Effects of hypoxia on function and morphology of in vitro frog gastric mucosa.

The effects of gaseous hypoxia and reoxygenation on oxynticopeptic (OPC) and surface mucous cells (SMC) were examined in in vitro bullfrog gastric fundic mucosae mounted in Ussing chambers. Forskolin-stimulated H+ secretion, transmucosal potential difference (PD), and electrical resistance (R) were monitored in tissues incubated in HCO3(-)-free or HCO3(-)-containing buffer. At serosal pH (pHs) 7.2, 1 h of hypoxia with 100% N2 resulted in a decrease in PD, increase in R, and complete inhibition of H+ secretion. After 30 min of hypoxia, the morphology of OPC changed from the secretory to the nonsecretory state without recognizable cytopathology. Destructive changes in OPC increased progressively at pHs 7.2 as the hypoxic period was prolonged from 4 to 24 h. After 4 h of reoxygenation following 12-24 h of hypoxia, OPC remained necrotic and H+ secretion showed no recovery, whereas in some areas where SMC were exfoliated adjacent SMC showed epithelial restitution. The recovery of H+ secretion and PD during 2 h of reoxygenation after 4 h of hypoxia at pHs 6.0 and 6.8 was less than that at 7.2 and 8.0 and was greater in the presence of serosal HCO3- than its absence at pHs 7.2. These results suggest that, in in vitro frog gastric mucosa, 1) OPC are more vulnerable to hypoxia than SMC, 2) basolateral acidosis exaggerates hypoxic injury of OPC, and 3) serosal HCO3- protects OPC from hypoxic injury.

Animals↗
PubMed1992

Basolateral K+ conductances in surface epithelium of Necturus antrum: effects of Ca2+ and divalent cations.

Intracellular microelectrode techniques were used to characterize basolateral membrane K+ conductances in isolated Necturus antral mucosa. Exposure of tissues to progressively higher levels of serosal K+ (4, 20, 40, or 60 mM) resulted in progressively greater depolarizations of basolateral membrane potentials and decreases in membrane resistance, consistent with the presence of a significant K+ conductance. Ba2+ (2 mM) partially blocks these conductances. Exposure of tissues to increased levels of serosal Ca2+ (from 1.8 to 6.8 mM) elicited significant hyperpolarization of basolateral potentials and decreases in basolateral resistance. These effects are also elicited by Sr2+ (5 mM), but not by Mg2+ (5 mM). Ba2+ (5 mM) elicits complex and time-dependent effects, but transiently elicits an effect similar to high Ca2+. Ion substitutions in the serosal perfusate suggest that the Ca(2+)-induced effects are due to enhancement of basolateral K+ conductances. Further work is necessary to identify the processes that mediate this increase in basolateral K+ conductance and to evaluate the physiological significance of this change in membrane permeability to K+.

Animals↗
PubMed1994

Brush-border tyrosine phosphorylation stimulates ileal neutral NaCl absorption and brush-border Na(+)-H+ exchange.

The drug genistein, a tyrosine (Tyr) kinase inhibitor, was used to define a role for Tyr phosphorylation in regulation of basal and stimulated neutral NaCl absorption in rabbit ileum. Brush-border vesicles contain Tyr-phosphorylated peptides. Genistein freeze-thawed into the vesicles caused a concentration-dependent inhibition of at least three peptides with M(r) 111,000, 83,000, and 80,000. Studied with the Ussing chamber-voltage clamp technique, genistein added to the ileal mucosal surface inhibited neutral NaCl absorption. Direct addition of genistein to brush-border vesicles made from ileal villus cells inhibited brush-border Na(+)-H+ exchange but not D-glucose-stimulated Na+ uptake. These effects were not duplicated by genistin, a drug with similar structure to genistein but lacking Tyr kinase inhibiting properties. Serosal but not mucosal epidermal growth factor (EGF) stimulated NaCl absorption. Mucosal genistein but not genistin also altered second-messenger regulation of neutral NaCl absorption, inhibiting the effect of Ca2+ ionophore A-23187 and of serosal EGF but not affecting the transport changes caused by 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP). In contrast, the Cl secretory effects indicated by the increase in short-circuit current for all three agents, A-23187, EGF, and 8-BrcAMP, were inhibited by mucosal genistein. These results suggest that 1) a Tyr kinase is involved in basally stimulating ileal neutral NaCl absorption and brush-border Na(+)-H+ exchange; 2) EGF stimulates NaCl absorption by an effect exerted from the serosal surface, but the effect also involves a brush-border Tyr kinase; 3) brush-border Tyr kinase is involved in the ability of Ca2+ ionophore A-23187 to inhibit neutral NaCl absorption but is not involved in the transport effects of cAMP. This study suggests that Tyr kinase(s) acting over short time periods is involved in stimulation of neutral NaCl absorption and brush-border Na(+)-H+ exchange and also in Ca(2+)-induced inhibition of NaCl absorption. These studies represent the first example of a brush-border Tyr kinase being involved in short-term signal transduction in intestinal epithelial cells.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1996

Effects of potassium on magnesium transport across rumen epithelium.

Increasing ruminal K concentration impairs active Mg transport across the forestomach epithelium of ruminants. We used Ussing chamber and microelectrode techniques to test the hypothesis that high mucosal K decreases the driving force for Mg2+ uptake by depolarizing the apical membrane. Serosal Ba enhanced net 42K secretion. Under open-circuit conditions, rumen epithelial cells showed an apical membrane potential (Va) of -67.3 +/- 1.5 mV. An increase in mucosal K concentration depolarized Va and decreased mucosal-to-serosal 28 Mg flux (Jm-->sMg). An increase in the transepithelial potential difference (Vt) depolarized Va, greatly decreased Jm-->sMg, and slightly increased Mg serosal-to-mucosal flux (Js-->mMg). Jm-->sMg exhibited an electrogenic and an electroneutral component. Mucosal verapamil depolarized Va and reduced Jm-->sMg, without affecting Js-->mMg. The study shows that rumen epithelial cells exhibit apical and basolateral K conductances and that transcellular Mg absorption has a distinct electrogenic component. This supports the assumption that a change in Va represents the link between increased ruminal K concentration and decreased Mg absorption. The results are discussed with regard to the development of hypomagnesemia in ruminants.

Animals↗
PubMed1998

Stanniocalcin: a novel protein regulating calcium and phosphate transport across mammalian intestine.

Stanniocalcin (STC) is an anti-hypercalcemic glycoprotein hormone previously identified in the corpuscles of Stannius in bony fish and recently in the human genome. This study undertook to express human STC in Chinese hamster ovary (CHO) cells and to determine its effects on calcium and phosphate absorption in swine and rat intestine. Unidirectional mucosal-to-serosal (Jm-->s) and serosal-to-mucosal (Js-->m) 45Ca and 32P fluxes were measured in vitro in duodenal tissue in voltage-clamped Ussing chambers. Addition of STC (10-100 ng/ml) to the serosal surface of the duodenum resulted in a simultaneous increase in calcium Jm-->s and Js-->m fluxes, with a subsequent reduction in net calcium absorption. This was coupled with an STC-stimulated increase in phosphate absorption. Intestinal conductance was increased at the highest dose of STC (100 ng/ml) in swine tissue. The addition of STC to the mucosal surface had no effect on calcium and phosphate fluxes. STC at doses of 10-1,000 ng/ml had no effect on short-circuit current in any region of the rat intestine. In conclusion, human recombinant STC decreases the absorption of calcium and stimulates the absorption of phosphate in both swine and rat duodenum. STC is a novel regulatory protein that regulates mammalian intestinal calcium and phosphate transport.

Animals↗
PubMed1998

Segment-specific effects of epinephrine on ion transport in the colon of the rat.

The effect of epinephrine on transport of K+, Na+, Cl-, and HCO-3 across the rat colon was studied using the Ussing chamber technique. Epinephrine (5 x 10(-6) mol/l) induced a biphasic change in short-circuit current (Isc) in distal and proximal colon: a transient increase followed by a long-lasting decay. The first phase of the Isc response was abolished in Cl--poor solution or after bumetanide administration, indicating a transient induction of Cl- secretion. The second phase of the response to epinephrine was suppressed by apical administration of the K+ channel blocker, quinine, and was concomitant with an increase in serosal-to-mucosal Rb+ flux, indicating that epinephrine induced K+ secretion, although this response was much smaller than the change in Isc. In addition, the distal colon displayed a decrease in mucosal-to-serosal and serosal-to-mucosal Cl- fluxes when treated with epinephrine. In the distal colon, indomethacin abolished the first phase of the epinephrine effect, whereas the second phase was suppressed by TTX. In the proximal colon, indomethacin and TTX were ineffective. The neuronally mediated response to epinephrine in the distal colon was suppressed by the nonselective beta-receptor blocker, propranolol, and by the beta2-selective blocker, ICI-118551, whereas the epithelial response in the proximal colon was suppressed by the nonselective alpha-blocker, phentolamine, and by the selective alpha2-blocker, yohimbine. These results indicate a segment-specific action of epinephrine on ion transport: a direct stimulatory action on epithelial alpha2-receptors in the proximal colon and an indirect action on secretomotoneurons via beta2-receptors in the distal colon.

Adrenergic Agonists↗
PubMed1999

Regulation of intracellular pH gradients by identified Na/H exchanger isoforms and a short-chain fatty acid.

Colonic luminal short-chain fatty acids (SCFA) stimulate electroneutral sodium absorption via activation of apical Na/H exchange. HT29-C1 cells were used previously to demonstrate that transepithelial SCFA gradients selectively activate polarized Na/H exchangers. Fluorometry and confocal microscopy (with BCECF and carboxy SNARF-1, respectively) are used to measure intracellular pH (pHi) in HT29-C1 cells, to find out which Na/H exchanger isoforms are expressed and if results are due to pHi gradients. Inhibition of Na/H exchange by HOE-694 identified 1) two inhibitory sites [50% inhibitory dose (ID50) = 1.6 and 0.05 microM] in suspended cells and 2) one inhibitory site each in the apical and basolateral membranes of filter-attached cells (apical ID50 = 1.4 microM, basolateral ID50 = 0.3 microM). RT-PCR detected mRNA of Na/H exchanger isoforms NHE1 and NHE2 but not of NHE3. Confocal microscopy of filter-attached cells reported HOE-694-sensitive pHi recovery in response to luminal or serosal 130 mM propionate. Confocal analysis along the apical-to-basal axis revealed that 1) luminal or serosal propionate establishes transcellular pHi gradients and 2) the predominant site of pHi acidification and pHi recovery is the apical portion of cells. Luminal propionate produced a significantly greater acidification of the apical vs. basal portion of the cell (compared with serosal propionate), but no other dependence on the orientation of the SCFA gradient was observed. Results provide direct evidence for a subcellular response that assures robust activation of apical NHE2 and dampening of basolateral NHE1 during pHi regulation.

Benzopyrans↗
PubMed1999

Effect of heat stress on rabbit esophageal epithelium.

Hot beverages expose the esophageal epithelium to temperatures as high as 58 degrees C. To study the impact of such temperatures, rabbit esophageal epithelium was exposed to luminal heat or both luminal and serosal heat while mounted in Ussing chambers. Luminal heat, mimicking exposure to hot beverages, reduced potential difference (PD) and resistance (R) when applied at >/=49 degrees C and reduced short-circuit current (Isc) at >/=60 degrees C. At >/=60 degrees C, subepithelial blisters developed. Higher temperatures reduced R only moderately and reversibly. In contrast, the Isc declined sharply and irreversibly once threshold was reached. Luminal and serosal heat also reduced PD, Isc, and R, although the threshold for reduction in Isc was now similar to that for R. Additionally, luminal and serosal heat reduced Isc more than R for any given temperature and resulted in blisters at lower temperatures (50 degrees C) than luminal heat alone. The heat-induced decline in Isc was attributed in part to inactivation of Na-K-ATPase activity, although other transport systems could have been equally affected, and the decline in R to an increase in paracellular permeability. The latter effect on R also contributed to an increase in tissue sensitivity to luminal acid damage. Consumption of hot beverages exposes the esophagus to temperatures that can negatively impact epithelial structure and function. Impaired barrier function by heat increases the risk of esophageal damage by subsequent contact with (refluxed) gastric acid. These findings help explain in part the association between esophageal disease and consumption of hot beverages.

Animals↗
PubMed2001

P2Y(11), a purinergic receptor acting via cAMP, mediates secretion by pancreatic duct epithelial cells.

Pancreatic duct epithelial cells (PDEC) mediate the exocrine secretion of fluid and electrolytes. We previously reported that ATP and UTP interact with P2Y(2) receptors on nontransformed canine PDEC to increase intracellular free Ca2+ concentration ([Ca2+](i)) and stimulate Ca2+-activated Cl- and K+ channels. We now report that ATP interacts with additional purinergic receptors to increase cAMP and activate Cl- channels. ATP, 2-methylthio-ATP, and ATP-gamma-S stimulated a 4- to 10-fold cAMP increase with EC(50) of 10-100 microM. Neither UTP nor adenosine stimulated a cAMP increase, excluding a role for P2Y(2) or P1 receptors. Although UTP stimulated an (125)I(-) efflux that was fully inhibited by 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetra(acetoxymethyl) ester (BAPTA-AM), ATP stimulated a partially resistant efflux, suggesting activation of additional Cl- conductances through P2Y(2)-independent and Ca2+-independent pathways. In Ussing chambers, increased cAMP stimulated a much larger short-circuit current (I(sc)) increase from basolaterally permeabilized PDEC monolayers than increased [Ca2+](i). Luminal ATP and UTP and serosal UTP stimulated a small Ca2+-type I(sc) increase, whereas serosal ATP stimulated a large cAMP-type I(sc) response. Serosal ATP effect was inhibited by P2 receptor blockers and unaffected by BAPTA-AM, supporting ATP activation of Cl- conductances through P2 receptors and a Ca2+-independent pathway. RT-PCR confirmed the presence of P2Y(11) receptor mRNA, the only P2Y receptor acting via cAMP.

Adenosine Triphosphate↗
PubMed1975

Water and ion transport by the urinary bladder of the teleost Pseudopleuronectes americanus.

Water and ion transport by the isolated teleost urinary bladder were studied. The transepithelial electrical PD across sac-type bladder preparations was unstable, i.e., initially mucosa positive but becoming more negative with time. Perfused bladders maintained a low mucosa positive PD which was stable. Both Na and Cl appeared to be actively transported from mucosal side (M) to serosal side (S). Voltage clamping the bladder at 0, -50, or +50 mV had almost no effect on active or passive Na or Cl flux in either direction. Na and Cl transport seemed electrically neutral. Fluid absorption (M to S) was directly correlated with absorption of osmotically active solutes. These solutes were almost all Na and Cl. The bladder acidified and secreted K+ into the mucosal fluid. Divalent ions were concentrated in the mucosal fluid as a result of fluid absorption. Although furosemide and ethacrynic acid inhibited ion and water transport by the bladder, ouabain was effective at a much lower concentration. Ouabain (10(-4) M) inhibited active Na transport when applied only to the mucosal or only to the serosal surface. Ouabain abolished the PD only from the serosal surface.

Animals↗
PubMed1975

Relations of weak-electrolyte transport and acid-base metabolism in rat small intestine in vitro.

The jejunal and ileal regions of rat small intestine in vitro exhibit different patterns of weak-electrolyte transport and acid-base metabolism. The jejunal pattern of weak-electrolyte transport is net transport of weak acids M yields S and of weak bases S yields M (M, mucosal; S, serosal), and the pattern of acid-base metabolism is luminal acidification and serosal alkalinization. In the absence of sodium or in the presence of metabolic inhibitors, weak-electrolyte transport and serosal alkalinization are inhibited, but luminal acidification is not inhibited. The ileal pattern of weak-electrolyte transport is the opposite of that of the jejunum and may be associated with the presence of a luminal alkalinization process observed in this region. In the absence of chloride the ileal patterns of weak-electrolyte transport and acid-base metabolism become similar to those of the jejunum. It is suggested that these observations support a previously proposed model for weak-electrolyte transport in the intestine consisting of a series three-compartment system in which the pH of the intermediate compartment is greater than that of the bulk phases.

Acetamides↗
PubMed1975

Effect of bile salts on amino acid transport by rabbit intestine.

The effect of bile salts on alanine absorption across four regional sites of rabbit intestine was examined using an in vivo single-pass perfusion technique. Na-deoxycholate at a concentration of 3 mM reduced alanine absorption across all levels of the intestine, and a higher concentration (10 mM) of Na-taurodeoxycholate (TDC) caused only a minimal reduction of alanine absorption in the jejunum. TDC, however, was more effective in in vitro experiments, causing an incrase in transmural serosal-to-mucosal flux of alanine and phenylalanine, particularly when present in both the mucosal and serosal media. It also reduced the mucosal-to-serosal alanine flux rate when present only in the mucosal medium. The influx of these amino acids across the mucosal brush border membrane was also decreased by TDC. These amino acid transport changes correlated fairly well with some observed histological changes of the intestinal epithelium. This suggests that bile salt inhibition of amino acid absorption is nonspecific in type and can be mainly explained as being the result of an injurious action of these surface-active agents on the rabbit intestine.

Alanine↗
PubMed1975

Mechanisms of disposal of acid and alkali in rabbit duodenum.

Stripped duodenal mucosa of rabbits was mounted in Ussing chambers containing a Ringer solution gassed with 100% O2. The disappearance of acid or alkali from the mucosal solution of short-circuited tissue was measured with a pH stat while the serosal pH was kept at 7.4. The duodenum rapidly disposed of both acid and alkali; neither property was altered by gassing with N2 while iodoacetate was in the perfusing solutions. Prevention of release of CO2 from the mucosal chamber obliterated the early rapid phase of acid disposal by the mucosa while a similar maneuver in the serosal chamber increased the appearance of serosal acid without altering the rate of acid disposal. Gut sacs of rabbit duodenum in vitro and in vivo showed a positive correlation between acid disposal and the rate of luminal CO2 production. While acid disposal progressively decreased with time for the in vitro gut sacs, the in vivo gut sac showed no fatigue in this respect. Luminal acidification in the Ussing chamber was associated with a profound reduction in short-circuit current (Isc), partially reversible by elevation of the mucosal pH but not by luminal glucose. Our data suggest that acid disposal occurs in part by intraluminal neutralization and in part by diffusion into the mucosa.

Acid-Base Equilibrium↗
PubMed1976

Ion transport across isolated antral mucosa of the rabbit.

Isotopic fluxes of Na, Cl, and K were measured across isolated antral mucosa under short-circuit conditions. HCO3 fluxes were also measured with either isotopic and/or pH-stat methods. Net secretion of all four ions was observed. HCO3 secretion is due to a transmural process requiring metabolic energy. Secretion of endogenous HCO3 was not observed, and the unidirectional mucosal-to-serosal flux of HCO3 was negligible. There appears to be a close relationship between HCO3 secretion and the unidirectional mucosal-to-serosal Cl flux, but not relationships were observed between the unidirectional serosal-to-mucosal flux or either unidirectional Na flux. The bulk of HCO3 secretion is independent of the unidirectional Cl fluxes, but there is a fraction of HCO3 transport that is dependent on unidirectional Cl transport. However, HCO3 transport is not measurably influenced by inhibition of net Cl (and Na) transport per se.

Acetylcholine↗