Bicarbonate and chloride transport across rat ileal basolateral membrane

1995 ◽  
Vol 51 (8) ◽  
pp. 799-803 ◽  
Author(s):  
M. Tosco ◽  
M. N. Orsenigo ◽  
A. Faelli
Keyword(s):  
Chloride Transport ◽  
Basolateral Membrane ◽  
Bicarbonate And Chloride Transport

Chloride transport by the cortical and outer medullary collecting duct

1987 ◽  
Vol 253 (2) ◽  
pp. F203-F212 ◽  
Author(s):  
V. L. Schuster ◽  
J. B. Stokes
Keyword(s):  
Chloride Transport ◽  
Collecting Duct ◽  
Exchange Process ◽  
Basolateral Membrane ◽  
Fine Tuning ◽  
Transport Systems ◽  
Acid Base ◽  
Intercalated Cell ◽  
Cl Channel ◽  
Collecting Tubule

The processes by which chloride is transported by the cortical and outer medullary collecting tubule have been most extensively studied using in vitro microperfusion of rabbit tubules. Chloride appears to be transported by three major mechanisms. First, Cl can be actively reabsorbed by an electroneutral Cl-HCO3 exchanger localized to the apical membrane of the HCO3-secreting (beta-type) intercalated cell. Cl exits this cell via a basolateral Cl channel. This anion exchange process can also operate in a Cl self-exchange mode, is stimulated acutely by beta-adrenergic agonists and cAMP, and is regulated chronically by in vivo acid-base status. Second, Cl can diffuse passively down electrochemical gradients via the paracellular pathway. Although this pathway does not appear to be selectively permeable to Cl, it is large enough to allow for significant passive reabsorption. Third, Cl undergoes recycling across the basolateral membrane of the H+-secreting (alpha-type) intercalated cell. HCO3 exit from this cell brings Cl into the cell via electroneutral Cl-HCO3 exchange; Cl then exits the cell via a Cl channel. Cl transport is thus required for acidification and alkalinization of the urine. Both of these processes exist in the cortical collecting tubule. Their simultaneous operation allows fine tuning of acid-base excretion. In addition, these transport systems, when functioning at equal rates, effect apparent electrogenic net Cl absorption without changing net HCO3 transport. These systems may play an important role in regulating Cl balance.

Mechanisms of sodium and chloride transport across equine tracheal epithelium

1990 ◽  
Vol 259 (6) ◽  
pp. L459-L467 ◽  
Author(s):  
G. J. Tessier ◽  
T. R. Traynor ◽  
M. S. Kannan ◽  
S. M. O3'Grady
Keyword(s):  
Chloride Transport ◽  
Short Circuit ◽  
Basolateral Membrane ◽  
Short Circuit Current ◽  
Ringer Solution ◽  
Tracheal Epithelium ◽  
Ussing Chambers ◽  
Cl Secretion ◽  
Cotransport System ◽  
Ethanesulfonic Acid

Equine tracheal epithelium, stripped of serosal muscle, mounted in Ussing chambers, and bathed in plasmalike Ringer solution generates a serosa-positive transepithelial potential of 10–22 mV and a short-circuit current (Isc) of 70–200 microA/cm2. Mucosal amiloride (10 microM) causes a 40–60% decrease in Isc and inhibits the net transepithelial Na flux by 95%. Substitution of Cl with gluconate resulted in a 30% decrease in basal Isc. Bicarbonate substitution with 20 mM N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid decreased the Isc by 21%. The Cl-dependent Isc was inhibited by serosal addition of 1 mM amiloride. Bicarbonate replacement or serosal amiloride (1 mM) inhibits the net Cl flux by 72 and 69%, respectively. Bicarbonate replacement significantly reduces the effects of serosal amiloride (1 mM) on Isc, indicating its effect is HCO3 dependent. Addition of 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP; 100 microM) causes a 40% increase in Isc. This effect is inhibited by subsequent addition of 10 microM serosal bumetanide. Bumetanide (10 microM) reduces net Cl secretion following stimulation with 8-BrcAMP (100 microM). Serosal addition of BaCl2 (1 mM) causes a reduction in Isc equal to that following Cl replacement in the presence or absence of 100 microM cAMP. These results suggest that 1) Na absorption depends on amiloride-inhibitable Na channels in the apical membrane, 2) Cl influx across the basolateral membrane occurs by both a Na-H/Cl-HCO3 parallel exchange mechanism under basal conditions and by a bumetanide-sensitive Na-(K?)-Cl cotransport system under cAMP-stimulated conditions, and 3) basal and cAMP-stimulated Cl secretion depends on Ba-sensitive K channels in the basolateral membrane.

Chloride Transport Across Rat Ileal Basolateral Membrane Vesicles

1992 ◽  
Vol 201 (3) ◽  
pp. 254-260 ◽  
Author(s):  
M. Daher ◽  
S. Acra ◽  
W. Dykes ◽  
F. K. Ghishan
Keyword(s):  
Chloride Transport ◽  
Basolateral Membrane ◽  
Membrane Vesicles ◽  
Basolateral Membrane Vesicles

SPI-0211 activates T84 cell chloride transport and recombinant human ClC-2 chloride currents

2004 ◽  
Vol 287 (5) ◽  
pp. C1173-C1183 ◽  
Author(s):  
John Cuppoletti ◽  
Danuta H. Malinowska ◽  
Kirti P. Tewari ◽  
Qiu-ju Li ◽  
Ann M. Sherry ◽  
...  
Keyword(s):  
Apical Membrane ◽  
Chloride Transport ◽  
Short Circuit ◽  
Basolateral Membrane ◽  
Adult Rabbit ◽  
Dependent Manner ◽  
T84 Cells ◽  
Hek 293 ◽  
Hek 293 Cells ◽  
293 Cells

The purpose of this study was to determine the mechanism of action of SPI-0211 (lubiprostone), a novel bicyclic fatty acid in development for the treatment of bowel dysfunction. Adult rabbit intestine was shown to contain mRNA for ClC-2 using RT-PCR, Northern blot analysis, and in situ hybridization. T84 cells grown to confluence on permeable supports were shown to express ClC-2 channel protein in the apical membrane. SPI-0211 increased electrogenic Cl− transport across the apical membrane of T84 cells, with an EC50 of ∼18 nM measured by short-circuit current ( Isc) after permeabilization of the basolateral membrane with nystatin. SPI-0211 effects on Cl− currents were also measured by whole cell patch clamp using the human embryonic kidney (HEK)-293 cell line stably transfected with either recombinant human ClC-2 or recombinant human cystic fibrosis transmembrane regulator (CFTR). In these studies, SPI-0211 activated ClC-2 Cl− currents in a concentration-dependent manner, with an EC50 of ∼17 nM, and had no effect in nontransfected HEK-293 cells. In contrast, SPI-0211 had no effect on CFTR Cl− channel currents measured in CFTR-transfected HEK-293 cells. Activation of ClC-2 by SPI-0211 was independent of PKA. Together, these studies demonstrate that SPI-0211 is a potent activator of ClC-2 Cl− channels and suggest a physiologically relevant role for ClC-2 Cl− channels in intestinal Cl− transport after SPI-0211 administration.

Sodium and chloride transport across the isolated porcine gallbladder

1989 ◽  
Vol 257 (1) ◽  
pp. C45-C51 ◽  
Author(s):  
S. M. O'Grady ◽  
P. J. Wolters
Keyword(s):  
Apical Membrane ◽  
Chloride Transport ◽  
Short Circuit ◽  
Basolateral Membrane ◽  
Short Circuit Current ◽  
Ringer Solution ◽  
Disulfonic Acid ◽  
Ussing Chambers ◽  
Cl Secretion ◽  
Conductive Pathway

Porcine gallbladder, stripped of serosal muscle, mounted in Ussing chambers, and bathed in plasma-like Ringer solution generates a serosal positive transepithelial potential of 4-7 mV and a short-circuit current (Isc) of 50-120 microA/cm2. Substitution of Cl with gluconate or HCO3 with N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) results in a 50% decrease in Isc. Treatment with 1 mM amiloride (mucosal side) or 0.1 mM acetazolamide (both sides) causes 25-27% inhibition of the Isc. Mucosal addition of 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid inhibits the Isc by 17%. Serosal addition of 0.1 mM bumetanide inhibits the Isc by 28%. Amiloride (1 mM) inhibits the net transepithelial fluxes of Na and Cl by 55 and 41%, respectively. Substitution of Cl with gluconate inhibits the net Na flux by 50%, whereas substitution of HCO3 with HEPES inhibits 85-90% of the net Na flux and changes Cl absorption to net secretion. Based on these results, it is hypothesized that Na and Cl transport across the apical membrane is mediated by two pathways, Na-H/Cl-HCO3 exchange and Na-HCO3 cotransport. Partial recycling of Cl and HCO3 presumably occurs through a Cl conductive pathway and Cl-HCO3 exchange, respectively, in the apical membrane. This results in net Na absorption, which accounts for most of the Isc observed under basal conditions. The effect of bumetanide on the basolateral membrane and the fact that Cl secretion occurs when HCO3 is absent suggests that Cl secretion involves a basolateral NaCl or Na-K-Cl cotransport system arranged in series with a Cl conductive pathway in the apical membrane.

BICARBONATE AND CHLORIDE TRANSPORT IN RELATION TO THE ACIDIFICATION OR ALKALINIZATION OF THE URINE

1980 ◽  
Vol 341 (1 Anion and Pro) ◽  
pp. 210-224 ◽  
Author(s):  
William A. Brodsky ◽  
John H. Durham ◽  
Gerhard Ehrenspeck
Keyword(s):  
Chloride Transport ◽  
Bicarbonate And Chloride Transport

Chloride transport in rabbit esophageal epithelial cells

2002 ◽  
Vol 282 (4) ◽  
pp. G663-G675 ◽  
Author(s):  
Solange Abdulnour-Nakhoul ◽  
Nazih L. Nakhoul ◽  
Canan Caymaz-Bor ◽  
Roy C. Orlando
Keyword(s):  
Epithelial Cells ◽  
Apical Membrane ◽  
Chloride Transport ◽  
Ussing Chamber ◽  
Basolateral Membrane ◽  
Rate Of Change ◽  
Luminal Cell ◽  
Transport Pathways ◽  
Basolateral Membranes ◽  
Esophageal Epithelial Cells

We investigated Cl− transport pathways in the apical and basolateral membranes of rabbit esophageal epithelial cells (EEC) using conventional and ion-selective microelectrodes. Intact sections of esophageal epithelium were mounted serosal or luminal side up in a modified Ussing chamber, where transepithelial potential difference and transepithelial resistance could be determined. Microelectrodes were used to measure intracellular Cl− activity (a[Formula: see text]), basolateral or apical membrane potentials ( V mBL or V mC), and the voltage divider ratio. When a basal cell was impaled, V mBL was −73 ± 4.3 mV and a[Formula: see text] was 16.4 ± 2.1 mM, which were similar in presence or absence of bicarbonate. Removal of serosal Cl−caused a transient depolarization of V mBL and a decrease in a[Formula: see text] of 6.5 ± 0.9 mM. The depolarization and the rate of decrease of a[Formula: see text] were inhibited by ∼60% in the presence of the Cl−-channel blocker flufenamate. Serosal bumetanide significantly decreased the rate of change of a[Formula: see text] on removal and readdition of serosal Cl−. When a luminal cell was impaled, V mC was −65 ± 3.6 mV and a[Formula: see text] was 16.3 ± 2.2 mM. Removal of luminal Cl− depolarized V mC and decreased a[Formula: see text] by only 2.5 ± 0.9 mM. Subsequent removal of Cl− from the serosal bath decreased a[Formula: see text]in the luminal cell by an additional 6.4 ± 1.0 mM. A plot of V mBL measurements vs. log a[Formula: see text]/log a[Formula: see text] (a[Formula: see text] is the activity of Cl− in a luminal or serosal bath) yielded a straight line [slope ( S) = 67.8 mV/decade of change in a[Formula: see text]/a[Formula: see text]]. In contrast, V mC correlated very poorly with log a[Formula: see text]/a[Formula: see text] ( S = 18.9 mV/decade of change in a[Formula: see text]/a[Formula: see text]). These results indicate that 1) in rabbit EEC, a[Formula: see text] is higher than equilibrium across apical and basolateral membranes, and this process is independent of bicarbonate; 2) the basolateral cell membrane possesses a conductive Cl− pathway sensitive to flufenamate; and 3) the apical membrane has limited permeability to Cl−, which is consistent with the limited capacity for transepithelial Cl− transport. Transport of Cl− at the basolateral membrane is likely the dominant pathway for regulation of intracellular Cl−.

scholarly journals Water transport in neonatal and adult rabbit proximal tubules

2002 ◽  
Vol 283 (2) ◽  
pp. F280-F285 ◽  
Author(s):  
Raymond Quigley ◽  
Michel Baum
Keyword(s):  
Water Transport ◽  
Water Permeability ◽  
Water Movement ◽  
Chloride Transport ◽  
Basolateral Membrane ◽  
Membrane Vesicles ◽  
Proximal Tubules ◽  
Adult Rabbit ◽  
Osmotic Gradient ◽  
Intracellular Compartment

We have recently demonstrated that although the osmotic water permeability ( P f) of neonatal proximal tubules is higher than that of adult tubules, the P f of brush-border and basolateral membrane vesicles from neonatal rabbits is lower than that of adults. The present study examined developmental changes in the water transport characteristics of proximal convoluted tubules (PCTs) in neonatal (9–16 days old) and adult rabbits to determine whether the intracellular compartment or paracellular pathway is responsible for the maturational difference in transepithelial water transport. The permeability of n-butanol was higher in the neonatal PCT than the adult PCT at all temperatures examined, whereas the diffusional water permeability was identical. Increasing the osmotic gradient increased volume absorption in both the neonatal and the adult PCT to the same degree. The P f was not different between the neonatal and the adult PCT at any osmotic gradient studied. To assess solvent drag as a measure of the paracellular transport of water, the effect of the osmotic gradient on mannitol and chloride transport were measured. There was no change in chloride or mannitol transport with the increased osmotic gradient in either group, indicating that there was no detectable paracellular water movement. In addition, the mannitol permeability of the neonatal PCT was found to be lower than that of the adult PCT with the isotonic bath (8.97 ± 4.01 vs. 40.49 ± 13.89 μm/s, P < 0.05). Thus the intracellular compartment of the neonatal PCT has a lower resistance for water transport than the adult PCT and is responsible for the higher than expected P f in the neonatal PCT.

Ion-secreting epithelia: chloride cells in the head region of Fundulus heteroclitus

1980 ◽  
Vol 238 (3) ◽  
pp. R185-R198 ◽  
Author(s):  
K. J. Karnaky
Keyword(s):  
Fundulus Heteroclitus ◽  
Chloride Transport ◽  
Basolateral Membrane ◽  
Freeze Fracture ◽  
Chloride Ion ◽  
Salt Gland ◽  
Chloride Cells ◽  
Head Region ◽  
Zonulae Occludentes ◽  
Apical Side

Transporting cells of ion-secreting epithelia are characterized by similar morphological patterns that include rich supplies of mitochondria, exotic patterns of surface amplification, and basolateral, plasma-membrane location of Na-K-ATPase, even though the direction of sodium transport across these epithelia is toward the apical side. Several new models for NaCl secretion propose that sodium, extruded into the intercellular space by Na-K-ATPase, reaches the apical side via the zonulae occludentes. Very recent freeze-fracture electron microscopy of avian salt gland and teleost chloride cells reveals that transporting cells are joined by simple, shallow zonulae occludentes. These observations lend morphological support to the concept that paracellular sodium ion permeation plays a central role in secretion. The chloride ion may traverse the epithelium via a transcellular route, entering the cell at the basolateral membrane by a chloride carrier linked to the cotransport of sodium down its electrochemical gradient into the cell. Finally, the chloride ion may exit the cell across the apical membrane by electrical forces. This review summarizes biochemical, morphological, and electrophysiological aspects of these new secretory models and the important contribution of a half century of research on teleost osmoregulatory mechanisms, including the chloride cell, to our understanding of sodium and chloride transport across secretory epithelia.

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