Gastric and duodenal HCO3- transport in vivo: influence of prostaglandins

1983 ◽  
Vol 245 (6) ◽  
pp. G751-G759 ◽  
Author(s):  
L. A. Smeaton ◽  
B. H. Hirst ◽  
A. Allen ◽  
A. Garner
Keyword(s):  
Prostaglandin E2 ◽  
Surface Area ◽  
Topical Application ◽  
Mammalian Species ◽  
Electrical Potential ◽  
Duodenal Mucosa ◽  
Electrical Potential Difference ◽  
Ph Stat

Gastric and duodenal HCO3- transport was compared in the same mammalian species (cat) in vivo. The most appropriate technique for detecting HCO3- in the lumen of the stomach was measurement of pH and CO2 tension, whereas in the duodenum it was pH-stat titration. For experiments on gastric HCO3- transport, conscious cats prepared with vagally denervated fundic pouches were used; for those on duodenal transport anesthetized animals with in situ perfused segments were studied. When expressed in terms of gross surface area, basal HCO3- output was six times greater in the duodenum than in the stomach (approximately 1.5 cf. approximately 0.25 mumol X cm-2 X 15 min-1). topical application of 16,16-dimethyl prostaglandin E2 (dmPGE2) to duodenal mucosa caused a concentration-dependent increase in HCO3- output and transmucosal electrical potential difference (PD) over the range 0.01–1.0 microgram X ml-1. PGE2 was approximately 200 times less potent than dmPGE2 as a stimulant of duodenal HCO3- transport. Increases in the rate of luminal HCO3- output following application of dmPGE2 were considerably less in the stomach compared with the duodenum (approximately 50% cf. approximately 1,000% at 1 microgram X ml-1). Intravenous dmPGE2 (1 microgram X kg-1 X h-1) had no effect on either gastric or duodenal HCO3- outputs. Indomethacin (5 mg X kg-1 iv) inhibited duodenal HCO3- output by approximately 50% and reduced PD but did not influence gastric HCO3- output. We propose that in the cat duodenum in vivo local prostaglandins regulate HCO3- transport, but in the cat stomach in vivo they have a less important role.

Inhibition of ion transport by bile salts in canine gastric mucosa

1976 ◽  
Vol 231 (5) ◽  
pp. 1433-1437 ◽  
Author(s):  
YJ Kuo ◽  
LL Shanbour
Keyword(s):  
Gastric Mucosa ◽  
Ion Transport ◽  
Bile Salts ◽  
Electrical Potential ◽  
Electrical Potential Difference ◽  
Ph Stat ◽  
Stat Method ◽  
Mucosal Side

Studies were conducted with in vivo and in vitro canine stomach preparations. Instillation of 5, 10, and 20 mM bile salts in TES bufer (pH 7.4) into the nonsecreting stomach in vivo caused a progressive decrease in electrical potential difference (PD) and an increase in electrical resitance (R). The rate of acid secretion, determined by the pH-stat method in the histamine-stimulated stomach, decreased with 5 and 20 mM bile salts. Mucosal adenosine triphosphate (ATP) content of the nonsecreting or secreting stomach was reduced by bile salts. In vitro flux studies demonstrated that within the first hour after 1 mM bile salts were added to the mucosal side of the chamber, PD decreased, R increased, and net sodium transport decreased. In the second hour, unidirectional fluxes of sodium increased, indicating an increase in permeability of the gastric mucosa to sodium. These results demonstrate that the initial action of bile salts is inhibition of ion transport, which is followed by an increase in permeability.

Surface epithelial HCO3(-) transport by mammalian duodenum in vivo

1982 ◽  
Vol 243 (5) ◽  
pp. G348-G358 ◽  
Author(s):  
G. Flemstrom ◽  
A. Garner ◽  
O. Nylander ◽  
B. C. Hurst ◽  
J. R. Heylings
Keyword(s):  
Prostaglandin E2 ◽  
Guinea Pigs ◽  
Epithelial Transport ◽  
Electrical Potential ◽  
Electrical Potential Difference ◽  
Continuous Exposure ◽  
Inhibitory Peptide ◽  
Major Mechanism ◽  
Direct Titration

Duodenal surface epithelial transport of HCO3(-) was measured by direct titration in anesthetized animals. Alkalinization of the lumen occurred in all species, although basal rates varied considerably: rats (approximately 10), cats (approximately 15), pigs (approximately 25), dogs (approximately 25), guinea pigs (approximately 40), and rabbits (approximately 170 mueq.cm-1.h-1). In cats duodenum transported HCO3(-) at a greater basal rate than jejunum (approximately 5 mueq.cm-2.h-1) and developed a higher transmucosal electrical potential difference (PD, lumen negative). Luminal application of 10 mM HCl for 5 min produced a sustained increase in the rate of duodenal HCO3(-) transport that was accompanied by a rise in appearance of E-like prostaglandin immunoreactivity in the lumen and a decrease in DNA release. In cats pretreated with indomethacin (10 mg/kg iv), acid caused only a transient increase in HCO3(-) transport. Exogenous prostaglandin E2 (1-12 microM, luminal) increased basal HCO3(-) transport in cats, rats, and dogs but had no effect on this transport in guinea pigs and rabbits. However, prostaglandin E2 increased HCO3(-) transport and PD in guinea pigs pretreated with inhibitors of tissue cyclooxygenase activity (indomethacin or aspirin) or gastric H+ secretion (cimetidine). Thus the continuous exposure of the duodenum of herbivores to HCl discharged from the stomach may itself stimulate HCO3(-) transport via an increase in endogenous prostaglandin levels and render exogenous prostaglandins ineffective. Secretin (1-15 CU/kg iv) was without effect in both cats and guinea pigs. In guinea pigs, intravenous glucagon (120-360 micrograms.kg-1.h-1) or gastric inhibitory peptide (5 micrograms/kg) both increased HCO3(-) transport but not PD. Hence, prostaglandin-stimulated and hormone-stimulated mechanisms of HCO3(-) transport probably occur in mammalian duodenum as found previously in the isolated amphibian duodenum. The results suggest that epithelial HCO3(-) transport is a major mechanism of acid disposal, and thus mucosal protection, in mammalian duodenum under the control of hormones and endogenous prostaglandins.

Active electrolyte transport in mammalian buccal mucosa

1988 ◽  
Vol 255 (3) ◽  
pp. G286-G291 ◽  
Author(s):  
R. C. Orlando ◽  
N. A. Tobey ◽  
V. J. Schreiner ◽  
R. D. Readling
Keyword(s):  
Buccal Mucosa ◽  
Short Circuit ◽  
Basolateral Membrane ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Electrolyte Transport ◽  
Electrical Potential Difference ◽  
Ussing Chambers ◽  
Net Fluxes

The transmural electrical potential difference (PD) was measured in vivo across the buccal mucosa of humans and experimental animals. Mean PD was -31 +/- 2 mV in humans, -34 +/- 2 mV in dogs, -39 +/- 2 mV in rabbits, and -18 +/- 1 mV in hamsters. The mechanisms responsible for this PD were explored in Ussing chambers using dog buccal mucosa. After equilibration, mean PD was -16 +/- 2 mV, short-circuit current (Isc) was 15 +/- 1 microA/cm2, and resistance was 1,090 +/- 100 omega.cm2, the latter indicating an electrically "tight" tissue. Fluxes of [14C]mannitol, a marker of paracellular permeability, varied directly with tissue conductance. The net fluxes of 22Na and 36Cl were +0.21 +/- 0.05 and -0.04 +/- 0.02 mueq/h.cm2, respectively, but only the Na+ flux differed significantly from zero. Isc was reduced by luminal amiloride, serosal ouabain, or by reducing luminal Na+ below 20 mM. This indicated that the Isc was determined primarily by active Na+ absorption and that Na+ traverses the apical membrane at least partly through amiloride-sensitive channels and exits across the basolateral membrane through Na+-K+-ATPase activity. We conclude that buccal mucosa is capable of active electrolyte transport and that this capacity contributes to generation of the buccal PD in vivo.

scholarly journals Transmural electrical potential difference in the mammalian esophagus in vivo

1978 ◽  
Vol 75 (2) ◽  
pp. 286-291 ◽  
Author(s):  
Keith S. Turner ◽  
Don W. Powell ◽  
Charles N. Carney ◽  
Roy C. Orlando ◽  
Eugene M. Bozymski
Keyword(s):  
Electrical Potential ◽  
Potential Difference ◽  
Electrical Potential Difference

scholarly journals Quantification method for timolol from in vivo samples for the development of a new glaucoma drug depot

2018 ◽  
Vol 4 (1) ◽  
pp. 225-227
Author(s):  
Thomas Eickner ◽  
Franziska Kopp ◽  
Andreas Brietzke ◽  
Sabine Kischkel ◽  
Stefan Oschatz ◽  
...  
Keyword(s):  
Drug Release ◽  
Topical Application ◽  
Aqueous Humour ◽  
Liquid Chromatography Mass Spectrometry ◽  
Timolol Maleate ◽  
Sustained Drug Release ◽  
Subconjunctival Space ◽  
New Zealand White Rabbits

AbstractGlaucoma is the second most common cause of blindness. An increased intraocular pressure is the only treatable symptom of glaucoma. Because patients often exhibit a poor therapy adherence, a drug depot consisting of ELA-NCO and hyaluronic acid with timolol was developed to ensure sustained drug release. This drug depot is formed by in situ polymerisation after injection into the subconjunctival space. To test the in vivo drug release of timolol in serum and aqueous humour, a liquid chromatography mass spectrometry (LCMS) method was developed and tested using spike- and recovery experiments, and on in vivo samples after topical application. Samples of serum and aqueous humour were taken from New Zealand White rabbits. For topical application, a commercially available formulation of timolol was used. This study presents results concerning the recovery of timolol from spiked samples. Serum and aqueous humour samples were spiked with timolol maleate to a final concentration of 50 ng/mL. Subsequently, the samples were extracted and analysed by LCMS. External calibration of the developed method showed high linearity. Recovery experiments showed no loss of timolol. Hence, the extraction method is robust and able to recover the whole amount of timolol from aqueous humour and serum.

Sodium transport and the cellular sodium transport pool of colonic epithelium: effects of sodium loading, aldosterone and lithium

1987 ◽  
Vol 112 (2) ◽  
pp. 247-252 ◽  
Author(s):  
C. J. Edmonds ◽  
J. Mackenzie
Keyword(s):  
Epithelial Cells ◽  
Sodium Transport ◽  
Time Course ◽  
Electrical Potential ◽  
Electrical Potential Difference ◽  
Active Sodium ◽  
Prolonged Infusion ◽  
Sodium Loading ◽  
Sodium Flux

ABSTRACT The cellular sodium transport pool and sodium transepithelial fluxes were investigated in vivo in rat distal colon in relation to sodium loading by intravenous infusion (3·5 h), and to short (4 h) and prolonged (72 h) i.v. administration of aldosterone. Considerable natriuresis and increase in body sodium content were produced by the sodium load but there was no significant effect on the transcellular sodium flux (active absorption from lumen to plasma) or on the sodium transport pool. Both short and prolonged aldosteronism produced similar increases in the transport pool and in the transcellular sodium flux, but the transepithelial electrical potential difference (p.d.) was significantly greater in rats given the prolonged infusion. Addition of amiloride to the solution in the lumen of the colon almost completely abolished the p.d., the transport pool and the transcellular sodium flux of the rats receiving prolonged infusion, but had much less effect in those given the short infusion. The time-course of recovery of p.d. following prolonged aldosteronism was similar to that described for the turnover rate of rat colonic epithelial cells. Lithium within the lumen had no significant effect in untreated rats but after prolonged aldosterone infusion lithium reduced the p.d. and the transcellular sodium flux although the transport pool was not reduced. These findings are consistent with the hypothesis that aldosteronism renders the apical membranes of the epithelial cells permeable to lithium and that intracellular accumulation of lithium depresses active sodium transfer. The observations are interpreted in terms of an epithelial model in which aldosterone induces amiloride-sensitive pathways (diffusion channels permeable to sodium and lithium) in the apical membrane which totally replace the amiloride-insensitive pathways when aldosteronism is prolonged; the resulting expansion of the sodium transport pool is the stimulus for increased active sodium transport across the basolateral membranes. J. Endocr. (1987) 112, 247–252

An Investigation of the Role of Possible Neural Mechanisms in Cholera Toxin-Induced Secretion in Rabbit Ileal Mucosa in Vitro

1989 ◽  
Vol 77 (2) ◽  
pp. 161-166 ◽  
Author(s):  
K. J. Moriarty ◽  
N. B. Higgs ◽  
M. Woodford ◽  
L. A. Turnberg
Keyword(s):  
Cholera Toxin ◽  
Fluid Transport ◽  
Short Circuit ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Electrical Potential Difference ◽  
Rabbit Ileum ◽  
Ileal Mucosa

1. Cholera toxin stimulates intestinal secretion in vitro by activation of mucosal adenylate cyclase. However, it has been proposed that cholera toxin promotes secretion in vivo mainly through an indirect mechanism involving enteric neural reflexes. 2. We examined this hypothesis further by studying the influence of neuronal blockade on cholera toxin-induced changes in fluid transport across rabbit ileum in vitro. Mucosa, stripped of muscle layers, was mounted in flux chambers and luminal application of crude cholera toxin (2 μg/ml) caused a delayed but sustained rise in the short-circuit current, electrical potential difference and Cl− secretion. Pretreatment with the nerve-blocking drug, tetrodotoxin (5 × 10−6 mol/l serosal side), failed to influence the secretory response to cholera toxin, and addition of tetrodotoxin at the peak response to cholera toxin also had no effect. 3. That tetrodotoxin could block neurally mediated secretagogues was confirmed by the demonstration that the electrical responses to neurotensin (10−7 mol/l and 10−8 mol/l) were blocked by tetrodotoxin (5 × 10−6 mol/l). Furthermore, the response to cholera toxin of segments of ileum, which included the myenteric, submucosal and mucosal nerve plexuses, was not inhibited by tetrodotoxin. 4. We conclude that cholera toxin-induced secretion in rabbit ileum in vitro is not mediated via a neurological mechanism.

scholarly journals Effects of cholecalciferol on the translocation of calcium by non-everted ileum in vitro

1975 ◽  
Vol 152 (2) ◽  
pp. 181-190 ◽  
Author(s):  
Eric S. Holdsworth ◽  
John E. Jordan ◽  
Ellen Keenan
Keyword(s):  
Sodium Dodecyl ◽  
Electrical Potential ◽  
Basement Membranes ◽  
Metabolic Energy ◽  
Temperature Sensitive ◽  
Mucosal Cell ◽  
Electrical Potential Difference ◽  
Mucosal Cells

An apparatus is described that allows perfusion of a non-everted segment of intestine in vitro and the study of the accumulation of substances within the mucosal cells. The translocation of Ca2+ by rachitic-chick ileum and the effect of pretreatment with cholecalciferol was investigated, with the following conclusions. (1) Entry of Ca2+ across the microvilli into mucosal cells is by diffusion; it does not require metabolic energy or the presence of any other inorganic ions. (2) Pretreatment of the chick with cholecalciferol causes increased permeability of the microvillus to Ca2+ in both directions (lumen to cell, cell to lumen). The increased transport brought about by cholecalciferol in vivo can be partially mimicked by sodium dodecyl sulphate added in vitro. (3) The sign and the magnitude of the electrical potential difference prevailing across the ileum does not influence Ca2+ transport. (4) Exit of Ca2+ from the mucosal cell is temperature-sensitive, requires metabolic energy and Na+. (5) Pretreatment with cholecalciferol caused increased movement of Ca2+ out of the cell across the basement membranes. This effect of cholecalciferol given in vivo could be markedly increased by the presence of dicyclohexylcarbodi-imide in the perfusion fluid. These observations suggested that cholecalciferol increased Ca2+ entry (and exit) at the mucosal surface and also caused Ca2+ to be more available to the pump at the serosal surface.

scholarly journals Electrical Potential Difference Measurements in Perfused Single Proximal Tubules of Necturus Kidney

1961 ◽  
Vol 44 (4) ◽  
pp. 679-687 ◽  
Author(s):  
Guillermo Whittembury ◽  
Erich E. Windhager
Keyword(s):  
Electrical Potential ◽  
Proximal Tubules ◽  
The Other ◽  
Potential Difference ◽  
Stopped Flow ◽  
Electrical Potential Difference ◽  
Necturus Maculosus ◽  
Other Hand ◽  
Glomerular Filtrate

Transtubular and peritubular face electrical potential differences (P.D.) of the proximal tubules of the kidney of the amphibian Necturus maculosus have been measured in situ. These measurements have been carried out both under normal conditions, when the tubular fluid originates in the glomerular filtrate, and under conditions when the composition of the tubular fluid has been altered using the stopped flow microperfusion technique. Under normal conditions the transtubular potential difference is 20 mv. (lumen-negative) and the P.D. across the peritubular face is 74 mv. (cell-negative). The P.D. across the luminal face is thus 54 mv. (cell-negative). This electrical asymmetry is not influenced by replacing the normal tubular fluid by NaCl, NaCl + mannitol, or by alteration in the intraluminal pH from 7 to 4. On the other hand, replacement of Na by K or choline and the addition of small amounts of DNP to the perfusate diminish this asymmetry.

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