Regulation of intracellular pH

2004 ◽  
Vol 28 (4) ◽  
pp. 160-179 ◽  
Author(s):  
Walter F. Boron
Keyword(s):  
Steady State ◽  
Intracellular Ph ◽  
Temperature Control System ◽  
Air Conditioner ◽  
Environmental Sensors ◽  
Animal Cells ◽  
Buffering Power ◽  
A Cell ◽  
Acid Extrusion ◽  
Acid Loading

The approach that most animal cells employ to regulate intracellular pH (pHi) is not too different conceptually from the way a sophisticated system might regulate the temperature of a house. Just as the heat capacity (C) of a house minimizes sudden temperature (T) shifts caused by acute cold and heat loads, the buffering power (β) of a cell minimizes sudden pHi shifts caused by acute acid and alkali loads. However, increasing C (or β) only minimizes T (or pHi) changes; it does not eliminate the changes, return T (or pHi) to normal, or shift steady-state T (or pHi). Whereas a house may have a furnace to raise T, a cell generally has more than one acid-extruding transporter (which exports acid and/or imports alkali) to raise pHi. Whereas an air conditioner lowers T, a cell generally has more than one acid-loading transporter to lower pHi. Just as a house might respond to graded decreases (or increases) in T by producing graded increases in heat (or cold) output, cells respond to graded decreases (or increases) in pHi with graded increases (or decreases) in acid-extrusion (or acid-loading) rate. Steady-state T (or pHi) can change only in response to a change in chronic cold (or acid) loading or chronic heat (or alkali) loading as produced, for example, by a change in environmental T (or pH) or a change in the kinetics of the furnace (or acid extrudes) or air conditioner (or acid loaders). Finally, just as a temperature-control system might benefit from environmental sensors that provide clues about cold and heat loading, at least some cells seem to have extracellular CO2 or extracellular HCO3− sensors that modulate acid-base transport.

scholarly journals Effect of basolateral CO2/HCO3- on intracellular pH regulation in the rabbit S3 proximal tubule.

1993 ◽  
Vol 102 (6) ◽  
pp. 1171-1205 ◽  
Author(s):  
N L Nakhoul ◽  
L K Chen ◽  
W F Boron
Keyword(s):  
Steady State ◽  
Proximal Tubule ◽  
Intracellular Ph ◽  
Ph Regulation ◽  
Uptake Mechanism ◽  
Luminal Membrane ◽  
S3 Segment ◽  
Acid Extrusion ◽  
Acid Loading

We used the absorbance spectrum of the pH-sensitive dye dimethylcarboxyfluorescein to monitor intracellular pH (pHi) in the isolated perfused S3 segment of the rabbit proximal tubule, and examined the effect on pHi of switching from a HEPES to a CO2/HCO3- buffer in the lumen and/or the bath (i.e., basolateral solution). Solutions were titrated to pH 7.40 at 37 degrees C. With 10 mM acetate present bilaterally (lumen and bath), this causing steady-state pHi to be rather high (approximately 7.45), bilaterally switching the buffer from 32 mM HEPES to 5% CO2/25 mM HCO3- caused a sustained fall in pHi of approximately 0.26. However, with acetate absent bilaterally, this causing steady-state pHi to be substantially lower (approximately 6.9), bilaterally switching to CO2/HCO3- caused a transient pHi fall (due to the influx of CO2), followed by a sustained rise to a level approximately 0.18 higher than the initial one. The remainder of the experiments was devoted to examining this alkalinization in the absence of acetate. Switching to CO2/HCO3- only in the lumen caused a sustained pHi fall of approximately 0.15, whereas switching to CO2/HCO3- only in the bath caused a transient fall followed by a sustained pHi increase to approximately 0.26 above the initial value. This basolateral CO2/HCO3(-)-induced alkalinization was not inhibited by 50 microM DIDS applied shortly after CO2/HCO3- washout, but was slowed approximately 73% by DIDS applied more than 30 min after CO2/HCO3- washout. The rate was unaffected by 100 microM bilateral acetazolamide, although this drug greatly reduced CO2-induced pHi transients. The alkalinization was not blocked by bilateral removal of Na+ per se, but was abolished at pHi values below approximately 6.5. The alkalinization was also unaffected by short-term bilateral removal of Cl- or SO4=. Basolateral CO2/HCO3- elicited the usual pHi increase even when all solutes were replaced, short or long-term (> 45 min), by N-methyl-D-glucammonium/glucuronate (NMDG+/Glr-). Luminal CO2/HCO3- did not elicit a pHi increase in NMDG+/Glr-. Although the sustained pHi increase elicited by basolateral CO2/HCO3- could be due to a basolateral HCO3- uptake mechanism, net reabsorption of HCO3- by the S3 segment, as well as our ACZ data, suggest instead that basolateral CO2/HCO3- elicits the sustained pHi increase either by inhibiting an acid-loading process or stimulating acid extrusion across the luminal membrane (e.g., via an H+ pump).

Intracellular pH transients in rat diaphragm muscle measured with DMO

1978 ◽  
Vol 235 (1) ◽  
pp. C49-C54 ◽  
Author(s):  
A. Roos ◽  
W. F. Boron
Keyword(s):  
Intracellular Ph ◽  
Weak Acid ◽  
Diaphragm Muscle ◽  
Disulfonic Acid ◽  
Free Solution ◽  
Rat Diaphragm ◽  
Control Value ◽  
Acid Load ◽  
Acid Extrusion ◽  
Acid Loading

Changes of the intracellular pH of rat diaphragm muscle were monitored at 30-min intervals with the weak acid DMO (5,5-dimethyl-2,4-oxazolidinedione). Transferring the muscle from a CO2-containing to a CO2-free solution caused intracellular pH (pHi) to rise by an average of 0.18 during the first 30 min and then to level off at a slightly lower value over the next 60-90 min. Transferring the muscle from a CO2-free to a CO2-containing solution caused pHi to fall by 0.18 during the first 30 min and then to recover by 0.05 over the next 90 min. Subsequent return to the CO2-free solution caused pHi to overshoot the control value by 0.10. Both the recovery and the overshoot can be accounted for by an acid-extruding pump. Intracellular acid loading with 118 mM DMO similarly caused pHi to fall initially, to recover slowly during the acid loading, and then to overshoot the control pHi on removal of the acid load. In the absence of HCO3-/CO2, acid extrusion was reduced by about a fifth. SITS (4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid) had no effect. The absence of either Na+ or Cl- from HCO3-/CO2- free solution reduced acid extrusion by about a half.

Acid extrusion in S3 segment of rabbit proximal tubule. I. Effect of bilateral CO2/HCO3-

1995 ◽  
Vol 268 (2) ◽  
pp. F179-F192 ◽  
Author(s):  
L. K. Chen ◽  
W. F. Boron
Keyword(s):  
Steady State ◽  
Proximal Tubule ◽  
Initial Rate ◽  
Iodoacetic Acid ◽  
Buffering Power ◽  
Acid Load ◽  
S3 Segment ◽  
Series Of Experiments ◽  
Acid Extrusion ◽  
Stimulation Of

Monitoring the absorbance spectra of the pH-sensitive dye dimethylcarboxyfluorescein, we studied intracellular pH (pHi) regulation in the isolated perfused S3 segment of rabbit proximal tubule. To explain a previous observation, that steady-state pHi is higher in the presence than in the absence of CO2/HCO3- (N. L. Nakhoul, L. K. Chen, and W. F. Boron. J. Gen. Physiol. 102: 1171-1205, 1993), we examined the effect of bilateral (i.e., luminal and basolateral) CO2/HCO3- on the acid extrusion processes responsible for recovery of pHi from acid loads. To compute fluxes from rates of pHi change, we determined the pHi dependence of intrinsic intracellular buffering power, which was approximately 50 mM/pH at pHi 6.5 and fell linearly to approximately 20 mM at pHi 7.4. In one series of experiments, we monitored the rate of pHi recovery from an acid load imposed by an NH4+/NH3 prepulse. Over a broad range of pHi values, total net acid extrusion was approximately four times higher in bilateral presence of CO2/HCO3- than in its absence. In a second group of experiments, which were designed to determine the effect of CO2/HCO3- on luminal Na+/H+ exchange, we monitored the rate of pHi recovery elicited by adding Na+ back to only the lumen, after first removing Na+ bilaterally. Initial rate of luminal Na(+)-dependent net acid extrusion in presence of CO2/HCO3- was approximately 229 microM/s (pHi 6.92), approximately 1.8 times higher than the flux of approximately 127 microM/s (P < 0.005) obtained in absence of CO2/HCO3- (pHi 6.66). CO2/HCO3- alkali-shifted the flux vs. pHi relationship by 0.3-0.4 pH units. In a final series of experiments, we examined the effect of CO2/HCO3- on the Na(+)-independent alkalinization that follows the rapid, initial acidification elicited by bilateral Na+ removal. In the presence of CO2/HCO3-, lag time for initiation of the Na(+)-independent alkalinization was only approximately 36 vs. approximately 211 s (P < 0.002) in absence of CO2/HCO3-. Also, Na(+)-independent net acid extrusion rate was approximately two to three times higher in presence than in absence of CO2/HCO3- at comparable pHi. This Na(+)-independent acid extrusion was insensitive to N-ethylmaleimide (2 mM), but was inhibited approximately 94% by efforts to deplete intracellular ATP (i.e., removal of glucose and amino acids, plus addition of 2 mM cyanide and 10 mM iodoacetic acid). Stimulation of luminal Na+/H+ exchange and Na(+)-independent acid extrusion appears to be the major, if not the entire, explanation for the higher steady-state pHi caused by bilateral addition of CO2/HCO3-.

scholarly journals Effect of eccentric contraction-induced injury on force and intracellular pH in rat skeletal muscles

2002 ◽  
Vol 92 (1) ◽  
pp. 93-99 ◽  
Author(s):  
E. W. Yeung ◽  
J.-P. Bourreau ◽  
D. G. Allen ◽  
H. J. Ballard
Keyword(s):  
Intracellular Ph ◽  
Eccentric Contraction ◽  
Eccentric Contractions ◽  
Optimal Length ◽  
Extrusion Rate ◽  
Reduction In Force ◽  
Buffering Power ◽  
Acid Load ◽  
Rat Soleus Muscle ◽  
Acid Extrusion

The effect of eccentric contraction on force generation and intracellular pH (pHi) regulation was investigated in rat soleus muscle. Eccentric muscle damage was induced by stretching muscle bundles by 30% of the optimal length for a series of 10 tetani. After eccentric contractions, there was reduction in force at all stimulation frequencies and a greater reduction in relative force at low-stimulus frequencies. There was also a shift of optimal length to longer lengths. pHi was measured with a pH-sensitive probe, 2′,7′-bis-(2-carboxyethyl)-5(6)-carboxyfluorescein AM. pHi regulation was studied by inducing an acute acid load with the removal of 20–40 mM ammonium chloride, and the rate of pHi recovery was monitored. The acid extrusion rate was obtained by multiplying the rate of pHi recovery by the buffering power. The resting pHi after eccentric contractions was more acidic, and the rate of recovery from acid load post-eccentric contractions was slower than that from postisometric controls. This is further supported by the slower acid extrusion rate. Amiloride slowed the recovery from an acid load in control experiments. Because the Na+/H+ exchanger is the dominant mechanism for the recovery of pHi, this suggests that the impairment in the ability of the muscle to regulate pHiafter eccentric contractions is caused by decreased activity of the Na+/H+ exchanger.

scholarly journals Regulation of intracellular pH in human neutrophils.

1985 ◽  
Vol 85 (3) ◽  
pp. 443-470 ◽  
Author(s):  
L Simchowitz ◽  
A Roos
Keyword(s):  
Intracellular Ph ◽  
Equilibrium Distribution ◽  
Human Peripheral Blood ◽  
Human Neutrophils ◽  
Intracellular Acidification ◽  
Control Value ◽  
Buffering Power ◽  
Blood Neutrophils ◽  
Acid Loading ◽  
Intracellular Alkalinization

The intracellular pH (pHi) of isolated human peripheral blood neutrophils was measured from the fluorescence of 6-carboxyfluorescein (6-CF) and from the equilibrium distribution of [14C]5,5-dimethyloxazolidine -2,4-dione (DMO). At an extracellular pH (pHo) of 7.40 in nominally CO2-free medium, the steady state pHi using either indicator was approximately 7.25. When pHo was suddenly raised from 7.40 to 8.40 in the nominal absence of CO2, pHi slowly rose by approximately 0.35 during the subsequent hour. A change of similar magnitude in the opposite direction occurred when pHo was reduced to 6.40. Both changes were reversible. Intrinsic intracellular buffering power, determined by using graded pulses of CO2 or NH4Cl, was approximately 50 mM/pH over the pHi range of 6.8-7.9. The course of pHi obtained from the distribution of DMO was followed during and after imposition of intracellular acid and alkaline loads. Intracellular acidification was brought about either by exposing cells to 18% CO2 or by prepulsing with 30 mM NH4Cl, while pHo was maintained at 7.40. In both instances, pHi (6.80 and 6.45, respectively) recovered toward the control value at rates of 0.029 and 0.134 pH/min. These rates were reduced by approximately 90% either by 1 mM amiloride or by replacement of extracellular Na with N-methyl-D-glucamine. Recovery was not affected by 1 mM SITS or by 40 mM alpha-cyano-4-hydroxycinnamate (CHC), which inhibits anion exchange in neutrophils. Therefore, recovery from acid loading is probably due to an exchange of internal H for external Na. Intracellular alkalinization was achieved by exposing the cells to 30 mM NH4Cl or by prepulsing with 18% CO2, both at a constant pHo 7.40. In both instances, pHi, which was 7.65 and 7.76, respectively, recovered to the control value. The recovery rates (0.033 and 0.077 pH/min, respectively) were reduced by 80-90% either by 40 mM CHC or by replacement of extracellular Cl with p-aminohippurate (PAH). SITS, amiloride, and ouabain (0.1 mM) were ineffective.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Role of Na-H exchangers and vacuolar H+ pumps in intracellular pH regulation in neonatal rat osteoclasts.

1995 ◽  
Vol 105 (2) ◽  
pp. 177-208 ◽  
Author(s):  
J H Ravesloot ◽  
T Eisen ◽  
R Baron ◽  
W F Boron
Keyword(s):  
Intracellular Ph ◽  
Imaging System ◽  
Ph Regulation ◽  
Neonatal Rat ◽  
Hill Coefficient ◽  
Acid Base ◽  
Buffering Power ◽  
Acid Extrusion

Osteoclasts resorb bone by pumping of H+ into a compartment between the cell and the bone surface. Intracellular pH (pHi) homeostasis requires that this acid extrusion, mediated by a vacuolar-type H+ ATPase, be complemented by other acid-base transporters. We investigated acid-extrusion mechanisms of single, freshly isolated, neonatal rat osteoclasts. Cells adherent to glass coverslips were studied in the nominal absence of CO2/HCO3-, using the pH-sensitive dye BCECF and a digital imaging system. Initial pHi averaged 7.31 and was uniform throughout individual cells. Intrinsic buffering power (beta 1) decreased curvilinearly from approximately 25 mM at pHi = 6.4 to approximately 6.0 mM at pHi = 7.4. In all polygonally shaped osteoclasts, and approximately 60% of round osteoclasts (approximately 20% of total), pHi recovery from acid loads was mediated exclusively by Na-H exchange. In these pattern-1 cells, pHi recovery was 95% complete within 200 s, and was blocked by removing Na+, or by applying 1 mM amiloride, 50 microM ethylisopropylamiloride (EIPA), or 50 microM hexamethyleneamiloride (HMA). The apparent K1/2 for HMA ([Na+]o = 150 mM) was 49 nM, and the apparent K1/2 for Na+ was 45 mM. Na-H exchange, corrected for amiloride-insensitive fluxes, was half maximal at pHi 6.73, with an apparent Hill coefficient for intracellular H+ of 2.9. Maximal Na-H exchange averaged 741 microM/s. In the remaining approximately 40% of round osteoclasts (pattern-2 cells), pHi recovery from acid loads was brisk even in the absence of Na+ or presence of amiloride. This Na(+)-independent pHi recovery was blocked by 7-chloro-4-nitrobenz-2-oxa-1,3-diazol (NBD-Cl), a vacuolar-type H+ pump inhibitor. Corrected for NBD-Cl insensitive fluxes, H+ pump fluxes decreased approximately linearly from 96 at pHi 6.8 to 11 microM/s at pHi 7.45. In approximately 45% of pattern-2 cells, Na+ readdition elicited a further pHi recovery, suggesting that H+ pumps and Na-H exchangers can exist simultaneously. We conclude that, under the conditions of our study, most neonatal rat osteoclasts express Na-H exchangers that are probably of the ubiquitous basolateral subtype. Some cells express vacuolar-type H+ pumps in their plasma membrane, as do active osteoclasts in situ.

scholarly journals Upregulated Na+/H+-Exchange Protects Human Colon Cancer Tissue against Intracellular Acidification

2019 ◽  
Vol 2019 ◽  
pp. 1-5 ◽  
Author(s):  
Ninna C. S. Voss ◽  
Henrik Kold-Petersen ◽  
Mikkel B. Henningsen ◽  
Casper Homilius ◽  
Ebbe Boedtkjer
Keyword(s):  
Colon Cancer ◽  
Steady State ◽  
Intracellular Ph ◽  
Human Colon ◽  
Cancer Tissue ◽  
Normal Colon ◽  
Colon Tissue ◽  
Colon Cancer Tissue ◽  
Human Colon Cancer ◽  
Acid Extrusion

Increased metabolism accelerates local acid production in cancer tissue. The mechanisms eliminating acidic waste products from human colon cancer tissue represent promising therapeutic targets for pharmacological manipulation in order to improve prognosis for the increasing number of patients with colon cancer. We sampled biopsies of human colonic adenocarcinomas and matched normal colon tissue from patients undergoing colon cancer surgery. We measured steady-state intracellular pH and rates of net acid extrusion in freshly isolated human colonic crypts based on fluorescence microscopy. Net acid extrusion was almost entirely (>95%) Na+-dependent. The capacity for net acid extrusion was increased and steady-state intracellular pH elevated around 0.5 in crypts from colon cancer tissue compared with normal colon tissue irrespective of whether they were investigated in the presence or absence of CO2/HCO3–. The accelerated net acid extrusion from the human colon cancer tissue was sensitive to the Na+/H+-exchange inhibitor cariporide. We conclude that enhanced net acid extrusion via Na+/H+-exchange elevates intracellular pH in human colon cancer tissue.

pH regulation in single glomerular mesangial cells. I. Acid extrusion in absence and presence of HCO3-

1988 ◽  
Vol 255 (6) ◽  
pp. C844-C856 ◽  
Author(s):  
G. Boyarsky ◽  
M. B. Ganz ◽  
R. B. Sterzel ◽  
W. F. Boron
Keyword(s):  
Steady State ◽  
Loading Rate ◽  
Mesangial Cells ◽  
Ph Regulation ◽  
Disulfonic Acid ◽  
Glomerular Mesangial Cells ◽  
Fluorescence Excitation ◽  
Dependent Transport ◽  
Acid Extrusion ◽  
Acid Loading

We have developed a technique to measure the fluorescence of a pH-sensitive dye (2,7-biscarboxyethyl-5(6)-carboxyfluorescein) in single glomerular mesangial cells in culture. The intracellular fluorescence excitation ratio of the dye was calibrated using the nigericin-high-K+ approach. In the absence of CO2-HCO3-, mesangial cells that are acid loaded by an NH+4 prepulse exhibit a spontaneous intracellular pH (pHi) recovery that is blocked either by ethylisopropylamiloride (EIPA) or removal of external Na+. This pHi recovery most probably reflects the activity of a Na+-H+ exchanger. When the cells are switched from a N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES)-buffered solution to one containing CO2-HCO3-, there is an abrupt acidification due to CO2 entry, which is followed by a spontaneous recovery of pHi to a steady-state value higher than that prevailing in HEPES. Both the rate of recovery and the higher steady-state pHi imply that the application of CO2-HCO3- introduces an increase in net acid extrusion from the cell. One third of total net acid extrusion in CO2-HCO3- is EIPA sensitive and most likely is mediated by the Na+-H+ exchanger. The remaining two thirds of acid extrusion could be caused by a decrease in the background acid-loading rate and/or the introduction of a new, HCO3- -dependent acid-extrusion mechanism. The HCO3- -induced alkalinization cannot be accounted for by a HCO3- -induced reduction in the acid-loading rate. The latter can be estimated by applying EIPA in the absence of HCO3- and observing the rate of pHi decline. We found that this acid-loading rate is only about one fifth as great as the total net acid extrusion rate in the presence of HCO3-. Indeed, two thirds of net acid extrusion in HCO3- is blocked by 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS), an inhibitor of HCO3- -dependent transport. Furthermore, the effects of EIPA and SITS were additive. Thus, in the presence of CO2-HCO3-, a SITS-sensitive-HCO3- -dependent transporter is the dominant mechanism of acid extrusion. This mechanism also accounts for the increase in steady-state pHi on addition of CO2-HCO3-.

scholarly journals Regulation of Intracellular pH in Single Rat Cortical Neurons in vitro: A Microspectrofluorometric Study

1993 ◽  
Vol 13 (5) ◽  
pp. 827-840 ◽  
Author(s):  
Yibing Ou-Yang ◽  
Pekka Mellergård ◽  
Bo K. Siesjö
Keyword(s):  
Steady State ◽  
Intracellular Ph ◽  
Cortical Neurons ◽  
Ph Sensitive ◽  
Disulfonic Acid ◽  
Extrusion Rate ◽  
Rat Cortical Neurons ◽  
Acid Extrusion

Intracellular pH (pHi) and the mechanisms of pHi regulation in cultured rat cortical neurons were studied with microspectrofluorometry and the pH-sensitive fluorophore 2′,7′-bis(carboxyethyl)-5,6-carboxyfluorescein. Steady-state pHi was 7.00 ± 0.17 (mean ± SD) and 7.09 ± 0.14 in nominally HCO3− -free and HCO3−-containing solutions, respectively, and was dependent on extracellular Na+ and Cl−. Following an acid transient, induced by an NH1 prepulse or an increase in CO2 tension, pHi decreased and then rapidly returned to baseline, with an average net acid extrusion rate of 2.6 and 2.8 mmol/L/min, in nominally HCO3− -free and HCO3− -containing solutions, respectively. The recovery was completely blocked by removal of extracellular Na+ and was partially inhibited by amiloride or 5- N-methyl- N-isobutylamiloride. In most cells pHi recovery was completely blocked in the presence of harmaline. The recovery of pHi was not influenced by addition of 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid (DIDS) or removal of Cl−. The rapid regulation of pHi seen following a transient alkalinization was not inhibited by amiloride or by removal of extracellular Na+, but was partially inhibited by DIDS and by removal of extracellular Cl−. The results are compatible with the presence of at least two different pHi-regulating mechanisms: an acid-extruding Na+/H+ antiporter, possibly consisting of different subtypes, and a passive Cl−/HCO3− exchanger, mediating loss of HCO3− from the cell.

Steady-state pHi, buffering power, and effect of CO2 in a smooth muscle-like cell line

1990 ◽  
Vol 258 (3) ◽  
pp. C461-C469 ◽  
Author(s):  
R. W. Putnam ◽  
R. D. Grubbs
Keyword(s):  
Smooth Muscle ◽  
Steady State ◽  
Cell Line ◽  
Intracellular Ph ◽  
Muscle Cells ◽  
Disulfonic Acid ◽  
Free Solution ◽  
Buffering Power ◽  
Ethanesulfonic Acid ◽  
External Ph

Intracellular pH (pHi) was studied in the smooth muscle-like cell line, BC3H-1, using the pH-sensitive fluorescent dye 2',7'-bis(2-carboxyethyl)-5,6-carboxyfluorescein (BCECF). The initial pHi measured in 20 mM Na N-2-hydroxyethylpiperazine-N'-2 ethanesulfonic acid-buffered medium [NHB; external pH (pHo) 7.4, 37 degrees C] was 6.89 +/- 0.01 (n = 178). pHi was affected by changes in external pHo, pHi changing by approximately 70% of the change in pHo. The intrinsic buffering power (beta int) of these cells, measured either with NH4Cl or Na propionate pulses, is low for muscle cells, averaging approximately 10 mM/pH unit. Steady-state pHi of BC3H-1 cells in NHB acidified reversibly on exposure to 0.5 mM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS; 1.4 +/- 0.3 x 10(-4) pH/s), 1 mM amiloride (2.0 +/- 0.7 x 10(-4) pH/s), or Na-free solution (8.3 +/- 2.4 x 10(-4) pH/s) and alkalinized upon exposure to Cl-free solutions (9.7 +/- 2.2 x 10(-4) pH/s). Exposure of BC3H-1 cells to CO2-HCO3-buffered solutions resulted in a transient acidification followed by an alkalinization of 0.3-0.4 pH unit to a new steady-state pHi of 7.27 +/- 0.01 (n = 65). This new steady-state pHi acidified very slowly upon exposure to 1 mM amiloride (0.3 +/- 0.1 x 10(-4) pH/s), acidified more rapidly upon exposure to 0.5 mM DIDS (5.9 +/- 0.6 x 10(-4) pH/s) or Na-free solutions (9.8 +/- 1.0 x 10(-4) pH/s), and alkalinized on exposure to Cl-free solutions (24.5 +/- 1.3 x 10(-4) pH/s).(ABSTRACT TRUNCATED AT 250 WORDS)

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