Acidification mechanisms on the basolateral membrane of renal vesicles from the developing nephron

1990 ◽  
Vol 259 (3) ◽  
pp. F458-F465
Author(s):  
M. Baum
Keyword(s):  
Proximal Tubule ◽  
Voltage Clamp ◽  
Basolateral Membrane ◽  
Disulfonic Acid ◽  
Co2 Removal ◽  
Loop Of Henle ◽  
Base Exchange ◽  
Newborn Rabbit ◽  
Renal Vesicle

The present study examined acidification mechanisms on the basolateral membrane of the early renal vesicle, an undifferentiated ball of cells that will develop into parts of the glomerulus, proximal tubule, loop of Henle, and a portion of the distal convoluted tubule. Renal vesicles were dissected from newborn rabbit kidneys and bathed in vitro. To examine the basolateral membrane acidification mechanisms, intracellular pH (pHi) was measured by use of the pH-sensitive dye (2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. Evidence for Cl(-)-base exchange included the fact that removal of bath Cl-resulted in cell alkalinization (7.35 +/- 0.03 to 7.48 +/- 0.05; P less than 0.01). Cell alkalinization induced by Cl- removal was also observed in presence of a voltage clamp without bath Na+ (7.18 +/- 0.02 to 7.39 +/- 0.04; P less than 0.01) and was inhibited by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). pHi recovery after acute alkalinization resulting from CO2 removal was 0.20 +/- 0.03 pH units/min in the presence of Cl-, 0.07 +/- 0.01 in experiments with 0.2 mM DIDS, and 0.07 +/- 0.01 in absence of bath Cl-. The early renal vesicle also has a basolateral Na(+)-H+ antiporter. Removal of bath Na+ resulted in cell acidification (7.36 +/- 0.09 to 7.18 +/- 0.06; P less than 0.01), which was inhibited by 2 mM amiloride. Cell pH recovery after acute acidification (NH4Cl prepulse technique) was entirely dependent on bath Na+ and inhibited by amiloride. Thus the renal vesicle has basolateral membrane Na(+)-H+ and Cl(-)-base exchangers that can defend against cell acidification and alkalinization, respectively.

Effect of luminal chloride on cell pH in rabbit proximal tubule

1988 ◽  
Vol 254 (5) ◽  
pp. F677-F683 ◽  
Author(s):  
M. Baum
Keyword(s):  
Proximal Tubule ◽  
Intracellular Ph ◽  
Apical Membrane ◽  
Chloride Transport ◽  
Disulfonic Acid ◽  
Bathing Solution ◽  
Ph Change ◽  
Base Exchange ◽  
Proximal Tubular

The present in vitro microperfusion study examined whether apical membrane chloride transport is mediated by chloride-base exchange in the rabbit proximal convoluted (PCT) and proximal straight tubule (PST) by examining the effect of the addition of luminal chloride on intracellular pH. Intracellular pH was measured fluorometrically using the pH-sensitive dye 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein. In PCT initially perfused without chloride, changing the luminal perfusate to a high chloride (148 mM)-low bicarbonate (5 mM) solution simulating late proximal tubular fluid produced a cell acidification (7.56 +/- 0.06 to 7.52 +/- 0.06, P less than 0.02) when 1 mM formate was present in the perfusate and bathing solution. This acidification was inhibited by 0.5 mM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. This chloride-base exchange was not observed in the absence of formate, and neither acetate nor lactate produced the cell acidification observed with formate. Because the Na+-H+ antiporter could blunt a pH change, 2 mM amiloride was added to the luminal perfusate. While addition of luminal chloride produced a small cell acidification in the absence of formate (7.63 +/- 0.06 to 7.60 +/- 0.05, P less than 0.05), a much greater cell acidification was observed in the presence of 1 mM formate (7.69 +/- 0.05 to 7.58 +/- 0.06, P less than 0.01). Chloride-base exchange was only detected in the presence of formate in the PST. These studies demonstrate apical membrane chloride-base exchange in the presence of formate in the rabbit proximal tubule consistent with chloride-formate exchange.

scholarly journals Neonatal rabbit proximal tubule basolateral membrane Na+/H+antiporter and Cl−/base exchange

1999 ◽  
Vol 276 (6) ◽  
pp. R1792-R1797 ◽  
Author(s):  
Mehul Shah ◽  
Raymond Quigley ◽  
Michel Baum
Keyword(s):  
Proximal Tubule ◽  
Intracellular Ph ◽  
Apical Membrane ◽  
Basolateral Membrane ◽  
Fluorescent Dye ◽  
Adult Rabbit ◽  
Base Exchange ◽  
Straight Tubules ◽  
Exchange Activity

The present in vitro microperfusion study examined the maturation of Na+/H+antiporter and Cl−/base exchanger on the basolateral membrane of rabbit superficial proximal straight tubules (PST). Intracellular pH (pHi) was measured with the pH-sensitive fluorescent dye 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein in neonatal and adult superficial PST. Na+/H+antiporter activity was examined after basolateral Na+ addition in tubules initially perfused and bathed without Na+. Neonatal Na+/H+antiporter activity was ∼40% that of adult segment (9.7 ± 1.5 vs. 23.7 ± 3.2 pmol ⋅ mm−1 ⋅ min−1; P < 0.001). The effect of bath Cl− removal on pHi was used to assess the rates of basolateral Cl−/base exchange. In both neonatal and adult PST, the Cl−/base exchange activity was significantly higher in the presence of 25 mM[Formula: see text] than in the absence of[Formula: see text] and was inhibited by cyanide and acetazolamide, consistent with Cl−/[Formula: see text]exchange. The proton flux rates in the presence of bicarbonate in neonatal and adult tubules were 14.1 ± 3.6 and 19.5 ± 3.5 pmol ⋅ mm−1min−1, respectively ( P = NS), consistent with a mature rate of Cl−/[Formula: see text]exchanger activity in neonatal tubules. Basolateral Cl−/base exchange activity in the absence of CO2 and[Formula: see text], with luminal and bath cyanide and acetazolamide, was greater in adult than in neonatal PST and inhibited by bath DIDS consistent with a maturational increase in Cl−/OH−exchange. We have previously shown that the rates of the apical membrane Na+/H+antiporter and Cl−/base exchanger were approximately fivefold lower in neonatal compared with adult rabbit superficial PST. These data demonstrate that neonatal PST basolateral membrane Na+/H+antiporter and Cl−/base exchanger activities are relatively more mature than the Na+/H+antiporter and Cl−/base exchangers on the apical membrane.

Electrogenic Na/HCO3 cotransport across basolateral membrane of isolated perfused Necturus proximal tubule

1987 ◽  
Vol 253 (2) ◽  
pp. F340-F350 ◽  
Author(s):  
A. G. Lopes ◽  
A. W. Siebens ◽  
G. Giebisch ◽  
W. F. Boron
Keyword(s):  
Proximal Tubule ◽  
Liquid Membrane ◽  
Initial Rate ◽  
Basolateral Membrane ◽  
Proximal Tubules ◽  
Disulfonic Acid ◽  
Necturus Maculosus ◽  
Ethanesulfonic Acid ◽  
Ph Microelectrodes

This study was undertaken to determine whether the proximal tubule of the mud puppy Necturus maculosus possesses a basolateral Na/HCO3 cotransporter. We examined the effects on basolateral membrane potential (Vbl) and intracellular pH (pHi) of 1) lowering basolateral [HCO3-] at constant PCO2, and 2) replacing Na+ with N-methyl-D-glucamine. Vbl and pHi were measured with Ling-Gerard and liquid-membrane pH microelectrodes, respectively, in isolated tubules perfused in vitro. We found that decreasing basolateral [HCO3-] from 10 mM (pH 7.5) to 2 mM (pH 6.8) resulted in an immediate depolarization of 14.9 mV, and a pHi decrease of 0.35. SITS (4-acetamido-4'-isothiocyanostibene-2,2'-disulfonic acid, 0.5 mM) inhibited the HCO3-induced depolarization by 87% and inhibited the initial rate of the pHi decrease by 79%. Replacement of basolateral Na+ with N-methyl-D-glucamine resulted in an immediate depolarization of 11.3 mV, and a pHi decrease of 0.36. SITS inhibited the zero Na-induced depolarization by 86% and the initial rate of the pHi decrease by 81%. Nominal removal of basolateral HCO3- (replaced with N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid) inhibited the zero Na-induced depolarization by 64%, whereas nominal removal of Na+ inhibited the 2 mM HCO3-induced depolarization by 67%. Replacement of all basolateral Cl- with glucuronate did not inhibit the changes in Vbl induced by changing [HCO3-] or [Na+]. Observations similar to those described above have been made previously on Ambystoma proximal tubules, and attributed to an electrogenic Na/HCO3 cotransport mechanism that carries HCO3-, Na+, and net negative charge in the same direction. We conclude that Necturus proximal tubules possess a similar, if not identical, electrogenic Na/HCO3 cotransport mechanism.

Intracellular pH regulates Na(+)-independent Cl(-)-base exchange in JTC-12 (proximal tubule) cells

1990 ◽  
Vol 258 (4) ◽  
pp. F883-F892
Author(s):  
I. Fineman ◽  
D. Hart ◽  
E. P. Nord
Keyword(s):  
Steady State ◽  
Proximal Tubule ◽  
Intracellular Ph ◽  
Recovery Process ◽  
Disulfonic Acid ◽  
Base Line ◽  
Co2 Removal ◽  
Transport Pathway ◽  
Bathing Medium ◽  
Base Exchange

The role of an anion exchange pathway in the regulation of intracellular pH (pHi) under alkaline load and steady-state conditions and the modulation of this transporter by pHi was investigated in confluent monolayers of cloned JTC-12 cells, derived from monkey kidney proximal tubule. Regulation of pHi was fluorometrically monitored using the pH-sensitive probe, 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF). Monolayers in which pHi was rapidly elevated by removal of HCO3(-)-CO2 from the bathing medium demonstrated an absolute requirement for Cl- to recover toward base-line pHi. The recovery process proceeded in the absence of Na+, was inhibited 80% by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid, and was unaffected by 10(-4) M amiloride. When extracellular pH (pHo) was serially lowered from 7.4 to 6.7, recovery from an alkaline load induced by removal of HCO3(-)-CO2 from the medium occurred only when pHi was elevated above approximately 7.25. Below pHi approximately 7.25 no recovery toward initial pHi was observed. When pHi was elevated above approximately 7.25 with pHo maintained at 6.7, the recovery process ceased at pHi approximately 7.25 despite favorably oriented Cl- and OH- chemical gradients. Consistent with these observations, removal of Cl- from the medium of cells buffered with 25 mM HCO3(-)-5% CO2 at pHo 7.4 (in the absence of Na+) resulted in reversible elevation of pHi, whereas in a solution buffered to pHo 6.7 with 5 mM HCO3(-)-5% CO2, removal of Cl- failed to elevate pHi. Under steady-state conditions in the presence of 25 mM HCO3(-)-5% CO2 at pHo 7.4, pHi was 7.40 +/- 0.02 and reversibly decreased to 7.23 +/- 0.01 on removal of Na+ (in the presence of amiloride) from the bathing medium, indicating that the Cl(-)-base exchanger is operative under basal conditions and functions as a base extruder. In summary the JTC-12 cell possesses a Na(+)-independent Cl(-)-base exchange mechanism that is operative under alkaline load and steady-state conditions. pHi but not pHo modulates the activity of this transport pathway, and below pHi approximately 7.25 the exchanger is quiescent.

Luminal flow rate regulates proximal tubule H-HCO3 transporters

1992 ◽  
Vol 262 (1) ◽  
pp. F47-F54 ◽  
Author(s):  
P. A. Preisig
Keyword(s):  
Proximal Tubule ◽  
Flow Rate ◽  
Initial Rate ◽  
Apical Membrane ◽  
Basolateral Membrane ◽  
Rate Dependence ◽  
Unstirred Layer ◽  
Disulfonic Acid ◽  
Luminal Flow

In vivo microperfusion was used to examine the mechanism of luminal flow rate dependence of proximal tubule acidification. Luminal flow rate was acutely changed between 5 and 40 nl/min, while luminal and peritubular capillary composition were held constant. With inhibition of basolateral membrane base transport by peritubular 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), cell pH (pHi) provides a sensitive index of apical membrane H secretory activity. At a luminal perfusate [HCO3] of 25 mM, progressive increases in luminal flow rate (5----15----25----40 nl/min) caused progressive increases in pHi. This effect was of a smaller magnitude with a luminal perfusate [HCO3] of 60 mM and was further decreased at a luminal perfusate [HCO3] of 100 mM. This pattern of diminished flow rate dependence at higher luminal [HCO3] is consistent with the presence of a luminal unstirred layer, whose composition can be modified by luminal flow rate. The activity of the apical membrane Na-H antiporter, assayed as the initial rate of pHi recovery from an acid load in the presence of peritubular DIDS, was faster at 40 compared with 5 nl/min. Basolateral membrane Na-3HCO3 symporter activity, assayed as the initial rate of pHi recovery from an alkali load in the absence of luminal and peritubular chloride, was faster at 40 compared with 5 nl/min. This effect was eliminated by luminal amiloride, suggesting an indirect effect of flow mediated by changes in pHi secondary to flow rate-dependent changes in apical membrane Na-H antiporter activity. In summary, increases in luminal flow rate directly increase apical membrane H secretion, possibly by modification of a luminal unstirred layer.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanism of bicarbonate exit across basolateral membrane of rabbit proximal straight tubule

1987 ◽  
Vol 252 (1) ◽  
pp. F11-F18 ◽  
Author(s):  
S. Sasaki ◽  
T. Shiigai ◽  
N. Yoshiyama ◽  
J. Takeuchi
Keyword(s):  
Negative Charge ◽  
Driving Forces ◽  
Basolateral Membrane ◽  
Disulfonic Acid ◽  
Exit Mechanism ◽  
Total Replacement ◽  
Straight Tubules ◽  
Proximal Straight Tubule ◽  
Basolateral Membrane Potential

To clarify the mechanism(s) of HCO3- (or related base) transport across the basolateral membrane, rabbit proximal straight tubules were perfused in vitro, and intracellular pH (pHi) and Na+ activity (aiNa) were measured by double-barreled ion-selective microelectrodes. Lowering bath HCO3- from 25 to 5 mM at constant PCO2 depolarized basolateral membrane potential (Vbl), and reduced pHi. Most of these changes were inhibited by adding 1 mM 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS) to the bath. Total replacement of bath Na+ with choline also depolarized Vbl and reduced pHi, and these changes were also inhibited by SITS. Reduction in aiNa was observed when bath HCO3- was lowered. Taken together, these findings suggest that HCO3- exists the basolateral membrane with Na+ and negative charge. Calculation of the electrochemical driving forces suggests that the stoichiometry of HCO3-/Na+ must be larger than two for maintaining HCO3- efflux. Total replacement of bath Cl- with isethionate depolarized Vbl gradually and increased pHi slightly, implying the existence of a Cl(-)-related HCO3- exit mechanism. The rate of decrease in pHi induced by lowering bath HCO3- was slightly reduced (20%) by the absence of bath Cl-. Therefore, the importance of Cl(-)-related HCO3- transport is small relative to total basolateral HCO3- exit. Accordingly, these data suggest that most of HCO3- exits the basolateral membrane through the rheogenic Na+/HCO3- cotransport mechanism with a stoichiometry of HCO3-/Na+ of more than two.

Electroneutral H+ secretion in distal tubule of Amphiuma

1987 ◽  
Vol 252 (4) ◽  
pp. F691-F699 ◽  
Author(s):  
B. Stanton ◽  
A. Omerovic ◽  
B. Koeppen ◽  
G. Giebisch
Keyword(s):  
Basolateral Membrane ◽  
Apical Cell ◽  
Distal Tubule ◽  
Cell Types ◽  
Disulfonic Acid ◽  
Type I ◽  
Cellular Mechanisms ◽  
Apical Cell Membrane ◽  
Membrane Type

This study examines the cellular mechanisms of acid secretion by the in vitro perfused late distal tubule of Amphiuma kidney. Acidification of tubule fluid occurred against an electrochemical gradient of 16 mV; thus H+ secretion was active. Amiloride (1 mM) or a reduction of sodium in the perfusion fluid (from 83.7 to 7.7 mM) partially reduced acidification. Amiloride, in the presence of low sodium, completely inhibited acidification. Furthermore, acetazolamide and ouabain in the bath solution (0.1 mM) also inhibited acidification. Conductive properties of the epithelium and of individual cell membranes were determined by means of cable analysis of the tubule and intracellular voltage recordings. The transepithelial voltage and resistance averaged -0.4 +/- 0.4 mV, lumen negative, and 7,147 +/- 845 omega X cm, respectively. Two functionally different cell types were identified by intracellular microelectrodes. Type I cells had a basolateral membrane voltage (Vbl) of -67.7 mV. As determined by ion substitution experiments, the basolateral membrane was conductive to K+ and Cl-. This cell also had a 4-acetamido-4'-isothiocyanostilbene-2-2'-disulfonic acid (SITS)-sensitive Na+-dependent HCO3- exit pathway in the basolateral membrane. Type II cells had a Vbl of -76.1 mV (P less than 0.05 vs. type I) and the basolateral membrane was conductive to K+ and Cl- but not to HCO3-. HCO3- movement across the basolateral membrane in this cell may occur by electroneutral Cl- -HCO3- exchange. The apical cell membrane of both cell types did not contain measurable ionic conductances, as evidenced by a high value of apical membrane fractional resistance (0.98 +/- 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Functional characterization of alpha- and beta-intercalated cell types in rabbit cortical collecting duct

1991 ◽  
Vol 261 (3) ◽  
pp. F377-F385 ◽  
Author(s):  
H. Furuya ◽  
M. D. Breyer ◽  
H. R. Jacobson
Keyword(s):  
Collecting Duct ◽  
Basolateral Membrane ◽  
Functional Characterization ◽  
Cell Types ◽  
Disulfonic Acid ◽  
Cortical Collecting Duct ◽  
Electrical Measurements ◽  
Collecting Ducts

Single-cell electrical measurements and spectrophotometric determinations of intracellular pH were used to determine unique features of alpha- and beta-intercalated cells (alpha-IC, beta-IC) in in vitro perfused rabbit cortical collecting ducts (CCD). pHi rose in alpha-IC and fell in beta-IC after bath Cl- removal. Luminal Cl- removal did not change pHi of alpha-IC, but pHi of beta-IC rose by 0.36 +/- 0.01 pH units. Cl- concentration-dependent recovery of beta-IC pHi revealed a Cl- Km of 18.7 mM for the luminal Cl(-) -HCO3- exchanger. Measurements of basolateral membrane voltage (Vbl) also showed two IC cell types. Removal of luminal Cl- did not change Vbl in alpha-IC, whereas Vbl hyperpolarized by a mean of 73.2 +/- 3.5 mV in beta-IC. Reducing bath Cl- depolarized both alpha- and beta-IC Vbl. In alpha-IC a large repolarization of 39.8 +/- 5.2 mV followed acute depolarization after bath Cl- removal. Reducing bath HCO3- (constant CO2) had little effect on beta-IC Vbl, whereas alpha-IC Vbl depolarized by 5.2 +/- 0.7 mV. Reducing luminal HCO3- in the absence of luminal Cl- produced a 17.6 +/- 1.8 mV depolarization in beta-IC. This change was independent of luminal Na+ and was not blocked by luminal 10(-4) M 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). In beta-IC, Vbl was not altered by either bath or lumen DIDS in the presence of luminal Cl-. However, when luminal Cl- was removed, luminal DIDS reversibly depolarized Vbl by 9.6 +/- 2.9 mV.(ABSTRACT TRUNCATED AT 250 WORDS)

Cellular actions of cAMP on HCO3(-)-secreting cells of rabbit CCD: dependence on in vivo acid-base status

1994 ◽  
Vol 266 (4) ◽  
pp. F528-F535 ◽  
Author(s):  
C. Emmons ◽  
J. B. Stokes
Keyword(s):  
Anion Exchanger ◽  
Collecting Duct ◽  
Basolateral Membrane ◽  
Disulfonic Acid ◽  
Intercalated Cells ◽  
Cortical Collecting Duct ◽  
Acid Base ◽  
Acid Base Status

HCO3- secretion by cortical collecting duct (CCD) occurs via beta-intercalated cells. In vitro CCD HCO3- secretion is modulated by both the in vivo acid-base status of the animal and by adenosine 3',5'-cyclic monophosphate (cAMP). To investigate the mechanism of cAMP-induced HCO3- secretion, we measured intracellular pH (pHi) of individual beta-intercalated cells of CCDs dissected from alkali-loaded rabbits perfused in vitro. beta-Intercalated cells were identified by demonstrating the presence of an apical anion exchanger (cell alkalinization in response to removal of lumen Cl-). After 180 min of perfusion to permit decrease of endogenous cAMP, acute addition of 0.1 mM 8-bromo-cAMP or 1 microM isoproterenol to the bath caused a transient cellular alkalinization (> 0.20 pH units). In the symmetrical absence of either Na+, HCO3-, or Cl-, cAMP produced no change in pHi. Basolateral dihydrogen 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (0.1 mM) for 15 min before cAMP addition also prevented this alkalinization. In contrast to the response of cells from alkali-loaded rabbits, addition of basolateral cAMP to CCDs dissected from normal rabbits resulted in an acidification of beta-intercalated cells (approximately 0.20 pH units). The present studies demonstrate the importance of the in vivo acid-base status of the animal in the regulation of CCD HCO3- secretion by beta-intercalated cells. The results identify the possible existence of a previously unrecognized Na(+)-dependent Cl-/HCO3- exchanger on the basolateral membrane of beta-intercalated cells in alkali-loaded rabbits.

Basolateral membrane Cl−-, Na+-, and K+-coupled base transport mechanisms in rat MTALH

2002 ◽  
Vol 282 (4) ◽  
pp. F655-F668 ◽  
Author(s):  
Soline Bourgeois ◽  
Sandrine Massé ◽  
Michel Paillard ◽  
Pascal Houillier
Keyword(s):  
Basolateral Membrane ◽  
Disulfonic Acid ◽  
Thick Ascending Limb ◽  
Transport Mechanisms ◽  
Medullary Thick Ascending Limb ◽  
Bilateral Absence ◽  
Transepithelial Voltage ◽  
Intracellular Alkalinization ◽  
Cellular Acidification

Mechanisms involved in basolateral HCO[Formula: see text] transport were examined in the in vitro microperfused rat medullary thick ascending limb of Henle (MTALH) by microfluorometric monitoring of cell pH. Removing peritubular Cl− induced a cellular alkalinization that was inhibited in the presence of peritubular 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (DIDS) and blunted in the absence of external CO2/HCO[Formula: see text]. The alkalinization elicited by removing peritubular Cl−persisted in the bilateral absence of Na+, together with a voltage clamp. When studied in Cl−-free solutions, lowering peritubular pH induced a base efflux that was inhibited by peritubular DIDS or by the absence of external CO2/HCO[Formula: see text]. Removing peritubular Na+ elicited a cellular acidification that was accounted for by stimulation of a DIDS- and ethylisopropylamiloride (EIPA)-insensitive Na+-HCO[Formula: see text] cotransport and inhibition of a basolateral Na+/H+exchange. Increasing bath K+ induced an intracellular alkalinization that was inhibited in the absence of external CO2/HCO[Formula: see text]. At 2 mM, peritubular Ba2+, which inhibits the K+-Cl−cotransport, did not induce any change in transepithelial voltage but elicited a cellular alkalinization and inhibited K+-induced cellular alkalinization, consistent with the presence of a basolateral, electroneutral Ba2+-sensitive K+-Cl− cotransport that may operate as a K+-HCO[Formula: see text] cotransport. This cotransport was inhibited in the peritubular presence of furosemide, [(dihydroindenyl)oxy]alkanoic acid, 5-nitro-2-(3-phenylpropylamino)benzoate, or DIDS. At least three distinct basolateral HCO[Formula: see text] transport mechanisms are functional under physiological conditions: electroneutral Cl−/HCO[Formula: see text] exchange, DIDS- and EIPA-insensitive Na+-HCO[Formula: see text] cotransport, and Ba2+-sensitive electroneutral K+-Cl−(HCO[Formula: see text]) cotransport.

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