scholarly journals Cytoplasmic pH regulation in normal and abnormal neutrophils. Role of superoxide generation and Na+/H+ exchange.

1986 ◽  
Vol 261 (2) ◽  
pp. 512-514
Author(s):  
S Grinstein ◽  
W Furuya ◽  
W D Biggar
Keyword(s):  
Ph Regulation ◽  
Cytoplasmic Ph ◽  
Superoxide Generation

Rabbit esophageal cell cytoplasmic pH regulation: role of Na(+)-H+ antiport and Na(+)-dependent HCO3- transport systems

1992 ◽  
Vol 263 (3) ◽  
pp. G407-G413 ◽  
Author(s):  
T. J. Layden ◽  
L. Schmidt ◽  
L. Agnone ◽  
P. Lisitza ◽  
J. Brewer ◽  
...  
Keyword(s):  
Ph Regulation ◽  
Transport Systems ◽  
Disulfonic Acid ◽  
Cytoplasmic Ph ◽  
Solution Ph ◽  
Acetoxymethyl Ester ◽  
Pulse Technique ◽  
Glass Cover Slip ◽  
Rat Tail

Regulation of cytoplasmic pH (pHi) of esophageal cells assumes importance as these cells can be exposed to mucosally absorbed acid during gastroesophageal reflux episodes. In this study, we examined whether esophageal cells possess pHi transport systems. Esophageal cells were harvested utilizing a gentle trypsin technique that yielded 2-5 x 10(6) cells per esophagus. Cells were attached to a glass cover slip that had been pretreated with rat-tail collagen, and pHi was measured continuously in a spectrofluorometer utilizing 2',7'-bis(2-carboxyethyl)-5(-6)- carboxyfluoroscein acetoxymethyl ester as a pH-sensitive fluorescent probe. The basal pHi of cells exposed to a Na(+)-containing solution averaged 7.52 +/- 0.20 (n = 6). The pHi declined slightly but not significantly to 7.46 +/- 0.12 with the addition of 5% CO2 and 28 mM NaHCO3. When H2 4,4'-diisothiocyanatostilbene- 2,2'-disulfonic acid (DIDS; 0.5 mM) was added, pHi was unchanged. However, addition of 10(-4) M amiloride caused pHi to decrease to 7.29 +/- 0.18 (P less than 0.01). When cells were acidified (pHi 6.3-7.0) using a NH4Cl (20 mM) pulse technique, pHi was rapidly restored toward neutrality in the presence of a HCO3(-)-free external Na+ concentration ([Na+]o)-containing solution (pH units/min = 0.26 +/- 0.12; n = 8). Alkalinization was completely blocked with 10(-4) M amiloride. In the presence of 10(-4) M amiloride, 28 mM NaHCO3, and 5% CO2, acidified cells also alkalinized, although at a slower rate (0.11 +/- 0.04 pH units/min; n = 16).(ABSTRACT TRUNCATED AT 250 WORDS)

Cytoplasmic pH regulation in phorbol ester-activated human neutrophils

1986 ◽  
Vol 251 (1) ◽  
pp. C55-C65 ◽  
Author(s):  
S. Grinstein ◽  
W. Furuya
Keyword(s):  
Metabolic Pathways ◽  
Phorbol Esters ◽  
Ph Regulation ◽  
Human Neutrophils ◽  
Hexose Monophosphate ◽  
Cytoplasmic Ph ◽  
Extracellular Acidification ◽  
Hexose Monophosphate Shunt ◽  
Activated Neutrophils ◽  
Cytoplasmic Acidification

Activation of neutrophils by 12-O-tetradecanoylphorbol-13-acetate (TPA) is accompanied by an initial cytoplasmic acidification, followed by an alkalinizing phase due to Na+-H+ countertransport. The source of the acidification, which is fully expressed by activation with TPA in Na+-free or amiloride-containing media, was investigated. The acidification phase was detected also in degranulated and enucleated cytoplasts, ruling out a major contribution by the nucleus or secretory vesicles. Cytoplasmic acidification was found to be associated with an extracellular acidification, suggesting metabolic generation of H+. Two principal metabolic pathways are stimulated in activated neutrophils: the reduction of O2 by NADPH-oxidase and the hexose monophosphate shunt. A good correlation was found between the activity of these pathways and the changes in cytoplasmic pH. Inhibition of superoxide synthesis prevented the TPA-induced cytoplasmic acidification. Moreover, activation of the hexose monophosphate shunt with permeable NADPH-oxidizing agents (in the absence of TPA) also produced a cytoplasmic acidification. Cytoplasmic acidification was also elicited by exogenous diacylglycerol and by other beta-phorbol diesters, which are activators of the kinase, but not by unesterified phorbol or by alpha-phorbol diesters, which are biologically inactive. The results suggest that the cytoplasmic acidification induced by phorbol esters in neutrophils reflects accumulation of H+ liberated during the metabolic burst that follows activation.

scholarly journals The role of anions in pH regulation of Leishmania major promastigotes.

1994 ◽  
Vol 269 (23) ◽  
pp. 16254-16259 ◽  
Author(s):  
L. Vieira ◽  
A. Lavan ◽  
F. Dagger ◽  
Z.I. Cabantchik
Keyword(s):  
Leishmania Major ◽  
Ph Regulation

Intracellular pH regulation in rabbit S3 proximal tubule: basolateral Cl-HCO3 exchange and Na-HCO3 cotransport

1990 ◽  
Vol 258 (2) ◽  
pp. F371-F381 ◽  
Author(s):  
N. L. Nakhoul ◽  
L. K. Chen ◽  
W. F. Boron
Keyword(s):  
Proximal Tubule ◽  
Intracellular Ph ◽  
Initial Rate ◽  
Ph Regulation ◽  
Basolateral Membrane ◽  
Intracellular Ph Regulation ◽  
S3 Segment ◽  
Absorbance Spectra ◽  
Rule Out

We studied the role of basolateral HCO3- transport in the regulation of intracellular pH (pHi) in the isolated perfused S3 segment of the rabbit proximal tubule. pHi was calculated from absorbance spectra of the pH-sensitive dye dimethylcarboxyfluorescein. Solutions were normally buffered to pH 7.4 at 37 degrees C with 25 mM HCO3- 5% CO2. pHi fell by approximately 0.17 when luminal [HCO3-] was lowered to 5 mM at fixed PCO2 (i.e., reducing pH to 6.8) but by approximately 0.42 when [HCO3-] in the bath (i.e., basolateral solution) was lowered to 5 mM. The pHi decrease elicited by reducing bath [HCO3-] was substantially reduced by removal of Cl- or Na+, suggesting that components of basolateral HCO3- transport are Cl- and/or Na+ dependent. We tested for the presence of basolateral Cl-HCO3 exchange by removing bath Cl-. This caused pHi to increase by approximately 0.23, with an initial rate of approximately 100 X 10(-4) pH/s. Although the initial rate of this pHi increase was not reduced by removing Na+ bilaterally, it was substantially lowered by the nominal removal of HCO3- from bath and lumen or by the addition of 0.1 mM 4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS) to the bath. The results thus suggest that a Na-independent Cl-HCO3 exchanger is present at the basolateral membrane. We tested for the presence of basolateral Na-HCO3 cotransport by removing bath Na+. This caused pHi to fall reversibly by approximately 0.26 with initial rates of pHi decline and recovery being approximately 30 and approximately 41 X 10(-4) pH/s, respectively. Although the bilateral removal of Cl- had no effect on these rates, the nominal removal of HCO3- or the presence of DIDS substantially slowed the pHi changes. Thus, in addition to a Cl-HCO3 exchanger, the basolateral membrane of the S3 proximal tubule also appears to possess a Na-HCO3 cotransport mechanism. The data do not rule out the possibility of other basolateral HCO3- transporters.

Role of apical anion exchangers in ph, regulation in polarized rat distal colonic surface cells

2001 ◽  
Vol 120 (5) ◽  
pp. A530
Author(s):  
Krishnan Selvi ◽  
Vazhaikkurichi M. Rajendran ◽  
Satish K. Singh
Keyword(s):  
Ph Regulation ◽  
Anion Exchangers

Role of calcium and cAMP messenger systems in intracellular pH regulation of osteoblastic cells

1992 ◽  
Vol 262 (1) ◽  
pp. C111-C121 ◽  
Author(s):  
J. Green ◽  
C. R. Kleeman
Keyword(s):  
Anion Exchanger ◽  
Calcium Concentration ◽  
Ph Regulation ◽  
Second Messengers ◽  
Suppressive Effect ◽  
Osteoblastic Phenotype ◽  
Umr 106 ◽  
Dose Dependent ◽  
Cytosolic Acidification

We have recently shown that two mechanisms are involved in the regulation of pHi in the osteoblastic phenotype cell line UMR-106 (Na(+)-H+ antiporter and a Na(+)-independent Cl(-)-HCO 3(-)-OH- exchanger). In the present work, we used the pH-sensitive dye 2',7'-bis(2-carboxyethyl)-5,6-carboxyfluorescein as well as isotope fluxes to investigate the influence of second messengers on the activity of these transporters. Elevation in intracellular calcium concentration [( Ca2+]in) in UMR-106 cells (measured by fura-2 fluorescence) is followed by stimulation of the Cl(-)-HCO3- exchanger, leading to cytosolic acidification. Subsequently, cell alkalinization, mediated by the Na(+)-H+ exchanger, restores pHi to its resting value. An acute reduction in [Ca2+]in abruptly stops the activity of the anion exchanger while having no influence on the activity of the Na(+)-H+ exchanger. The stimulatory effect of Ca2+in on the anion exchanger is dose dependent and is abrogated by the calmodulin inhibitors N-(6-aminohexyl)-5-chloro-naphthalenesulfonamide and calmidazolium. An increase in intracellular adenosine 3',5'-cyclic monophosphate (cAMP) brought about by forskolin, 8-bromo-cAMP, or prostaglandin E2 leads to inhibition of activity of both the Na(+)-H+ antiporter and the anion exchanger. The suppressive effect of cAMP on Cl(-)-HCO3- exchange could be overcome by elevating [Ca2+]in. We conclude that 1) Ca2+in and cAMP can influence pHi in osteoblasts by altering the activities of pHi regulatory mechanisms and 2) the effect of Ca2+in is probably mediated by calmodulin.

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