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Journal articles on the topic 'PHi regulation'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

WALSH, PATRICK J. "Regulation of Intracellular pH by Toadfish (Opsanus Beta) Hepatocytes." Journal of Experimental Biology 147, no. 1 (1989): 407–19. http://dx.doi.org/10.1242/jeb.147.1.407.

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The BCECF [2′,7′-bis(carboxyethyl)-5(6)-carboxyfluorescein] method for measurement of intracellular pH (pHi) was successfully applied to toadfish (Opsanus beta Goode and Bean) hepatocytes and used for investigating the pHi regulatory properties of the hepatocytes. As in previous studies of fish hepatocytes, toadfish hepatocyte pHi showed a marked dependence on extracellular pH (pHe) with characteristic values of about 0.15–0.2 units below pHe. Measurement of membrane potential (−33.76±3.07mV, N=3) in toadfish hepatocytes by the S14CN− distribution method allowed calculation of equilibrium pHi

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2

Mellergard, P., Y. Ou-Yang, and B. K. Siesjo. "Relationship between intra- and extracellular pH in primary cultures of rat astrocytes." American Journal of Physiology-Cell Physiology 267, no. 2 (1994): C581—C589. http://dx.doi.org/10.1152/ajpcell.1994.267.2.c581.

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We studied the influence of extracellular pH (pHe) on the mechanisms regulating intracellular pH (pHi) in astrocytes cultured from neonatal rat cortex, using single cell microspectrofluorometry and the pH-sensitive fluorophore 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. When pHe was maintained at control values of 7.35 during acid transients caused by an increased CO2 tension, pHi was rapidly regulated back to normal. However, at pHe 6.9 or below, there was no recovery of pHi. Steady-state pHi was also strongly dependent on pHe (pHi = 1.14 + 0.80 pHe). The pHi recovery after normalizati

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3

Shartau, R. B., D. A. Crossley, Z. F. Kohl, R. M. Elsey, and C. J. Brauner. "American alligator (Alligator mississippiensis) embryos tightly regulate intracellular pH during a severe acidosis." Canadian Journal of Zoology 96, no. 7 (2018): 723–27. http://dx.doi.org/10.1139/cjz-2017-0249.

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Crocodilian nests naturally experience high CO2 (hypercarbia), which leads to increased blood Pco2 and reduced blood pH (pHe) in embryos; their response to acid–base challenges is not known. During acute hypercarbia, snapping turtle embryos preferentially regulate tissue pH (pHi) against pHe reductions. This is proposed to be associated with CO2 tolerance in reptilian embryos and is not found in adults. In the present study, we investigated pH regulation in American alligator (Alligator mississippiensis (Daudin, 1802)) embryos exposed to 1 h of hypercarbia hypoxia (13 kPa Pco2, 9 kPa Po2). Hyp

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4

Zhang, R. G., S. G. Kelsen, and J. C. LaManna. "Measurement of intracellular pH in hamster diaphragm by absorption spectrophotometry." Journal of Applied Physiology 68, no. 3 (1990): 1101–6. http://dx.doi.org/10.1152/jappl.1990.68.3.1101.

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The regulation of intracellular pH (pHi) is important in controlling muscle contraction. In these experiments, a spectrophotometric method of determining pHi was developed, and the method was then used to study muscle pHi regulation during CO2-induced changes in extracellular pH (pHb). Studies were performed in vitro on 27 diaphragm muscle strips obtained from adult hamsters. pHi was measured from the ratio of the absorbances of the acid (lambda = 530 nm) and alkaline (lambda = 460 nm) forms of a vital dye, neutral red, using the unstained diaphragm spectrum as a reference blank. A standard ne

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5

Mellergård, Pekka E., Yi-Bing Ouyang, and Bo K. Siesjö. "The regulation of intracellular pH in cultured astrocytes and neuroblastoma cells, and its dependence on extracellular pH in a HCO3-free solution." Canadian Journal of Physiology and Pharmacology 70, S1 (1992): S293—S300. http://dx.doi.org/10.1139/y92-275.

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Microspectrofluorometry was used to study the regulation of intracellular pH (pHi) in 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF)-loaded astrocytes and the neuroblastoma–glioma cells of the NG 108-15 line. The cells rapidly regulated pHi during an acid transient induced by an NH4+ prepulse. This regulation was blocked by removal of Na+, or by addition of 1 mM amiloride. The back regulation was also inhibited when extracellular pH (pHe) was lowered. Furthermore, when cells were exposed to buffer with reduced or increased pHe, pHi changed in parallel. Thus, although these cells pos

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6

McLean, Lee Anne, Jane Roscoe, Nanna K. Jørgensen, Fredric A. Gorin, and Peter M. Cala. "Malignant gliomas display altered pH regulation by NHE1 compared with nontransformed astrocytes." American Journal of Physiology-Cell Physiology 278, no. 4 (2000): C676—C688. http://dx.doi.org/10.1152/ajpcell.2000.278.4.c676.

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Malignant gliomas exhibit alkaline intracellular pH (pHi) and acidic extracellular pH (pHe) compared with nontransformed astrocytes, despite increased metabolic H+ production. The acidic pHe limits the availability of[Formula: see text], thereby reducing both passive and dynamic [Formula: see text]-dependent buffering. This implies that gliomas are dependent upon dynamic[Formula: see text]-independent H+buffering pathways such as the type 1 Na+/H+exchanger (NHE1). In this study, four rapidly proliferating gliomas exhibited significantly more alkaline steady-state pHi(pHi = 7.31–7.48) than norm

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7

Goldstein, Jonathan I., James M. Mok, Christopher M. Simon, and J. C. Leiter. "Intracellular pH regulation in neurons from chemosensitive and nonchemosensitive regions of Helix aspersa." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 2 (2000): R414—R423. http://dx.doi.org/10.1152/ajpregu.2000.279.2.r414.

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We used 2′,7′-bis(carboxyethyl)-5(6)-carboxyflourescein (BCECF), a pH-sensitive fluorescent dye, to study intracellular pH (pHi) regulation in neurons in CO2chemoreceptor and nonchemoreceptor regions in the pulmonate, terrestrial snail, Helix aspersa. We studied pHiduring hypercapnic acidosis, after ammonia prepulse, and during isohydric hypercapnia. In all treatment conditions, pHifell to similar levels in chemoreceptor and nonchemoreceptor regions. However, pHi recovery was consistently slower in chemoreceptor regions compared with nonchemoreceptor regions, and pHi recovery was slower in all

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8

Akiba, Yasutada, Jonathan D. Kaunitz, and Marshall H. Montrose. "CFTR and pHi regulation." American Journal of Physiology-Gastrointestinal and Liver Physiology 310, no. 11 (2016): G1183. http://dx.doi.org/10.1152/ajpgi.00133.2016.

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9

Durand, T., J. L. Gallis, S. Masson, P. J. Cozzone, and P. Canioni. "pH regulation in perfused rat liver: respective role of Na(+)-H+ exchanger and Na(+)-HCO3- cotransport." American Journal of Physiology-Gastrointestinal and Liver Physiology 265, no. 1 (1993): G43—G50. http://dx.doi.org/10.1152/ajpgi.1993.265.1.g43.

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Na(+)-H+ antiport and Na(+)-HCO3- symport are involved in intracellular pH (pHi) homeostasis in cultured hepatocytes. We have studied the occurrence of these transport systems in the intact rat liver by 31P nuclear magnetic resonance. Livers perfused with a Krebs medium (25 mM HCO3-, pH 7.4, 37 degrees C) displayed a cytosolic pH 7.18 +/- 0.05 (n = 32). In response to an acid load (35 mM isobutyric acid), pHi remained constant. The same result was obtained in the presence of 1 mM amiloride (with or without acid load), indicating that the amiloride-sensitive Na(+)-H+ exchanger is inactive at ex

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10

Mair, N., H. Moser, and F. Fresser. "CONTRIBUTION OF THE Na+/H+ ANTIPORTER TO THE REGULATION OF INTRACELLULAR pH IN A CRAYFISH STRETCH RECEPTOR NEURONE." Journal of Experimental Biology 178, no. 1 (1993): 109–24. http://dx.doi.org/10.1242/jeb.178.1.109.

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Regulation of intracellular pH (pHi) following acidosis induced by NH4+/NH3 exposures was re-investigated in a crayfish stretch receptor neurone using H+- and Na+-selective microelectrodes. All experiments were performed in nominally HCO3-/CO2-free salines. From studies in Na+-free saline and from electrochemical calculations, we concluded that pHi regulation was dependent on extracellular Na+ concentration ([Na+]o). The half-maximal rate of pHi recovery had an apparent Michaelis-Menten constant of 21 mmol l-1 [Na+]o. The use of this experimental approach and an improved technique enabled us t

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11

Kupriyanov, V. V., B. Xiang, B. Kuzio, and R. Deslauriers. "pH regulation of K+ efflux from myocytes in isolated rat hearts:87Rb,7Li, and31P NMR studies." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 1 (1999): H279—H289. http://dx.doi.org/10.1152/ajpheart.1999.277.1.h279.

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This study investigates the effects of intracellular (pHi) and extracellular pH (pHe) on the efflux of Rb+ and Li+ in isolated rat hearts.87Rb and7Li NMR were used to measure Rb+ and Li+ content, respectively, of hearts, and 31P NMR was used to monitor pHi, pHe, and phosphate levels. After 30-min equilibration with Rb+ or Li+, effluxes were initiated by switching perfusion to a Rb+- or Li+-free, high-K+ (20.7 mM) Krebs-Henseleit buffer with 15 μM bumetanide. Monensin (2 μM) increased pHi from 7.10 ± 0.05 to 7.32 ± 0.07 and resulted in activation of Rb+ efflux; the first-order rate constant ( k

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12

Boron, Walter F. "Regulation of intracellular pH." Advances in Physiology Education 28, no. 4 (2004): 160–79. http://dx.doi.org/10.1152/advan.00045.2004.

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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 f

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13

Wood, Chris M., and James N. Cameron. "Temperature and the Physiology of Intracellular and Extracellular Acid-Base Regulation in the Blue Crab Callinectes Sapidus." Journal of Experimental Biology 114, no. 1 (1985): 151–79. http://dx.doi.org/10.1242/jeb.114.1.151.

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The 14C-DMO/3H-inulin method for pHi was critically assessed in intact Callinectes and found to be reliable provided adequate equilibration time and significant radiolabel excretion were taken into account. An unusually high ‘mean whole body pHi’ (7.54 at 20°C compared with a pHa of 7.80) was due to a highly alkaline fluid compartment (pHi = 8.23) in the carapace. At 20°C the pHi of the heart was 7.35 and skeletal muscle pHi was 7.30, and there were small but consistent differences in the pHi of different muscle types. The change in pHa with temperature was −0.0151 u°C−1 between 10 and 30°C, s

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14

Oliveira, P. F., M. Sousa, A. Barros, T. Moura, and A. Rebelo da Costa. "Intracellular pH regulation in human Sertoli cells: role of membrane transporters." REPRODUCTION 137, no. 2 (2009): 353–59. http://dx.doi.org/10.1530/rep-08-0363.

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Sertoli cells are responsible for regulating a wide range of processes that lead to the differentiation of male germ cells into spermatozoa. Intracellular pH (pHi) is an important parameter in cell physiology regulating namely cell metabolism and differentiation. However, pHi regulation mechanisms in Sertoli cells have not yet been systematically elucidated. In this work, pHi was determined in primary cultures of human Sertoli cells. Sertoli cells were exposed to weak acids, which caused a rapid acidification of the intracellular milieu. pHi then recovered by a mechanism that was shown to be p

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15

Bevensee, Mark O., Regina A. Weed, and Walter F. Boron. "Intracellular pH Regulation in Cultured Astrocytes from Rat Hippocampus." Journal of General Physiology 110, no. 4 (1997): 453–65. http://dx.doi.org/10.1085/jgp.110.4.453.

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We studied the regulation of intracellular pH (pHi) in single cultured astrocytes passaged once from the hippocampus of the rat, using the dye 2′,7′-biscarboxyethyl-5,6-carboxyfluorescein (BCECF) to monitor pHi. Intrinsic buffering power (βI) was 10.5 mM (pH unit)−1 at pHi 7.0, and decreased linearly with pHi; the best-fit line to the data had a slope of −10.0 mM (pH unit)−2. In the absence of HCO3−, pHi recovery from an acid load was mediated predominantly by a Na-H exchanger because the recovery was inhibited 88% by amiloride and 79% by ethylisopropylamiloride (EIPA) at pHi 6.05. The ethylis

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16

Wuttke, W. A., T. Munsch, and M. S. Berry. "Intracellular pH of giant salivary gland cells of the leech Haementeria ghilianii: regulation and effects on secretion." Journal of Experimental Biology 189, no. 1 (1994): 179–98. http://dx.doi.org/10.1242/jeb.189.1.179.

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1. Intracellular pH (pHi) and membrane potential (Em) of giant salivary gland cells of the leech, Haementeria ghilianii, were measured with double-barrelled, neutral-carrier, pH-sensitive microelectrodes. 2. Em was -51 +/- 11.2 mV and pHi was 6.98 +/- 0.1 (mean +/- S.D., N = 41) in Hepes-buffered saline (nominally HCO3(-)-free; extracellular pH, pHe = 7.4). pHi was independent of Em. 3. Amiloride (2 mmol l-1) had no effect on resting pHi or on pHi recovery from an acid load (induced by the NH4+ pre-pulse technique). Removal of external Na+ produced a progressive acidification which was blocked

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17

FitzHarris, Greg, and Jay M. Baltz. "Regulation of intracellular pH during oocyte growth and maturation in mammals." REPRODUCTION 138, no. 4 (2009): 619–27. http://dx.doi.org/10.1530/rep-09-0112.

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Regulation of intracellular pH (pHi) is a fundamental homeostatic process essential for the survival and proliferation of virtually all cell types. The mammalian preimplantation embryo, for example, possesses Na+/H+and HCO3−/Cl−exchangers that robustly regulate against acidosis and alkalosis respectively. Inhibition of these transporters prevents pH corrections and, perhaps unsurprisingly, leads to impaired embryogenesis. However, recent studies have revealed that the role and regulation of pHiis somewhat more complex in the case of the developing and maturing oocyte. Small meiotically incompe

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18

Schoolwerth, A. C., B. C. Smith, and K. Drewnowska. "Regulation of glutamine metabolism in dog kidney cortex: effect of pH and chronic acidosis." American Journal of Physiology-Renal Physiology 262, no. 6 (1992): F1007—F1014. http://dx.doi.org/10.1152/ajprenal.1992.262.6.f1007.

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To examine the interrelationships of proton compartmentation and ammoniagenesis, experiments were performed in tubules and mitochondria isolated from dog kidney cortex. Tubules were incubated in Krebs-Henseleit buffer at different pH (pHe), and cytosolic pH (pHi) was estimated with the fluorescent probe 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. Mitochondrial pH (pHm) was determined simultaneously in intact tubules by use of dimethyloxazolidine-2,4-dione. Over the pHe range 6.9-7.7, pHi was similar in control and acidotic dogs and linearly related to pHe. At pHe 7.4 in control tubules.

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19

Lubman, R. L., and E. D. Crandall. "Regulation of intracellular pH in alveolar epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 262, no. 1 (1992): L1—L14. http://dx.doi.org/10.1152/ajplung.1992.262.1.l1.

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Alveolar type II epithelial cells in adult mammalian lungs actively transport salt and water, secrete surfactant, and differentiate into type I cells under normal conditions and following lung injury. It has become increasingly apparent that, like all epithelial cells, alveolar pneumocytes have evolved specialized ion transport mechanisms by which they regulate their intracellular pH (pHi). pHi is an important biological parameter in all living cells whose regulation is necessary for normal cellular homeostasis. pHi, and the ion transport mechanisms by which it is regulated, may contribute to

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20

Ou-Yang, Yibing, Pekka Mellergård, and Bo K. Siesjö. "Regulation of Intracellular pH in Single Rat Cortical Neurons in vitro: A Microspectrofluorometric Study." Journal of Cerebral Blood Flow & Metabolism 13, no. 5 (1993): 827–40. http://dx.doi.org/10.1038/jcbfm.1993.105.

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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/mi

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21

Shepherd, R. M., G. H. Williams, and S. J. Quinn. "Regulation of intracellular pH in single rat zona glomerulosa cells." American Journal of Physiology-Cell Physiology 262, no. 1 (1992): C182—C190. http://dx.doi.org/10.1152/ajpcell.1992.262.1.c182.

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The cytosolic pH (pHi) regulation of rat adrenal zona glomerulosa (ZG) cells was studied using single-cell spectrofluorimetry. Basal pHi was similar for cells incubated in the absence or presence of the HCO3(-)-CO2 buffering system. In the absence of HCO3-, inhibition of the Na(+)-H+ exchanger by dimethylamiloride (DMA) or removal of extracellular Na+ produced substantial acidification of basal pHi. In the presence of HCO3-, neither maneuver affected basal pHi. However, removing extracellular Cl- produced a prompt alkalinization not observed in the absence of HCO3-. Alkalinizing mechanisms wer

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22

Wray, S. "Smooth muscle intracellular pH: measurement, regulation, and function." American Journal of Physiology-Cell Physiology 254, no. 2 (1988): C213—C225. http://dx.doi.org/10.1152/ajpcell.1988.254.2.c213.

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Smooth muscle performs many functions that are essential for the normal working of the human body. Changes in pH are thought to affect many aspects of smooth muscle. Despite this, until recently little was known about either intracellular pH (pHi) values or pHi regulation in smooth muscle. Recent work measuring pHi with either microelectrodes or nuclear magnetic resonance spectroscopy is now providing some of this much needed information for smooth muscles. From these studies, it can be concluded tentatively that pHi is the same in different smooth muscles, approximately 7.06 (37 degrees C). T

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23

Montrose, M. H., and H. Murer. "Regulation of intracellular pH by cultured opossum kidney cells." American Journal of Physiology-Cell Physiology 259, no. 1 (1990): C110—C120. http://dx.doi.org/10.1152/ajpcell.1990.259.1.c110.

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Opossum kidney (OK) cells (an epithelial cell line) were examined by flame photometry of cellular Na+ and K+ and by microfluorometric measurements of the intracellular pH (pHi) of single cells loaded with 2',7'-bis(2-carboxyethyl)-5,6-carboxyfluorescein (BCECF). The work concentrates on defining resting pHi values under different experimental conditions and examines factors that contribute to the maintenance of resting pHi. To use nigericin to calibrate the intracellular response of BCECF, cellular K+ levels were measured by a null point analysis, and the stability and magnitude of cellular Na

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24

Harvey, B. J., and J. Ehrenfeld. "Role of Na+/H+ exchange in the control of intracellular pH and cell membrane conductances in frog skin epithelium." Journal of General Physiology 92, no. 6 (1988): 793–810. http://dx.doi.org/10.1085/jgp.92.6.793.

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Ion-sensitive microelectrodes and current-voltage analysis were used to study intracellular pH (pHi) regulation and its effects on ionic conductances in the isolated epithelium of frog skin. We show that pHi recovery after an acid load is dependent on the operation of an amiloride-sensitive Na+/H+ exchanger localized at the basolateral cell membranes. The antiporter is not quiescent at physiological pHi (7.1-7.4) and, thus, contributes to the maintenance of steady state pHi. Moreover, intracellular sodium ion activity is also controlled in part by Na+ uptake via the exchanger. Intracellular ac

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25

Ofori-Darko, E., and A. H. Tashjian. "Regulation of pHi in Saos-2 cells by thrombin: roles of proteolytic activity and cytosolic calcium transients." American Journal of Physiology-Cell Physiology 263, no. 6 (1992): C1266—C1273. http://dx.doi.org/10.1152/ajpcell.1992.263.6.c1266.

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Some, if not all, of the cellular actions of alpha-thrombin are now believed to be mediated by proteolytic cleavage of the cell surface thrombin receptor to yield a tethered ligand that initiates signal transduction via the receptor. We have investigated the actions of alpha-thrombin on the regulation of cytosolic free Ca2+ concentration ([Ca2+]i) and intracellular pH (pHi) in human osteoblast-like Saos-2 cells. After acidification with nigericin, thrombin induced an acute increase of [Ca2+]i and a rise in pHi. The action of thrombin on pHi was dependent on activation of the Na(+)-H+ antiporte

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26

Demaurex, N., G. P. Downey, T. K. Waddell, and S. Grinstein. "Intracellular pH regulation during spreading of human neutrophils." Journal of Cell Biology 133, no. 6 (1996): 1391–402. http://dx.doi.org/10.1083/jcb.133.6.1391.

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The regulation of the intracelluar pH (pHi) during spreading of human neutrophils was studied by a combination of fluorescence imaging and video microscopy. Spreading on adhesive substrates caused a rapid and sustained cytosolic alkalinization. This pHi increase was prevented by the omission of external Na+, suggesting that it results from the activation of Na+/H+ exchange. Spreading-induced alkalinization was also precluded by the compound HOE 694 at concentrations that selectively block the NHE-1 isoform of the Na+H+ antiporter. Inhibition of Na+/H+ exchange by either procedure unmasked a si

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27

Schlue, W. R., and R. Dörner. "The regulation of pH in the central nervous system." Canadian Journal of Physiology and Pharmacology 70, S1 (1992): S278—S285. http://dx.doi.org/10.1139/y92-273.

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The pHi regulation from intracellular acidosis in the central nervous system appears to be mediated by mechanisms driven by the large inwardly directed Na+ gradient. The involvement of these mechanisms in pHi regulation of neurones and glial cells has been investigated in the leech central nervous system using ion-selective microelectrodes. For recovery from acidification, there appear to be three separate mechanisms: Na+/H+ exchange, Na+-dependent Cl−/HCO3− exchange, and Na+–HCO3− cotransport. All three mechanisms have a profound effect on the maintenance of pHi homeostasis in glial ceils; wh

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28

Abrahamse, S. L., A. Vis, R. J. Bindels, and C. H. van Os. "Regulation of intracellular pH in crypt cells from rabbit distal colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 267, no. 3 (1994): G409—G415. http://dx.doi.org/10.1152/ajpgi.1994.267.3.g409.

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H+ secretory mechanisms and intrinsic intracellular buffering capacity were studied in crypt cells from rabbit distal colon. To this end crypts of Lieberkuhn were isolated by microdissection, and intracellular pH (pHi) was measured using digital imaging fluorescence microscopy and the pH-sensitive fluorescent dye 2',7'-bis(2-carboxyethyl)- 5(6)-carboxyfluorescein. In the absence of HCO(3-)-CO2 and presence of Na+, resting pHi was 7.51 +/- 0.04 (n = 237/23, cells/crypts). However, 6 min after superfusion with a solution containing zero Na+, 1 x 10(5) M Sch-28080 and 5 x 10(-8) M bafilomycin A1,

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29

Liu, S., D. Piwnica-Worms, and M. Lieberman. "Intracellular pH regulation in cultured embryonic chick heart cells. Na(+)-dependent Cl-/HCO3- exchange." Journal of General Physiology 96, no. 6 (1990): 1247–69. http://dx.doi.org/10.1085/jgp.96.6.1247.

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The contribution of Cl-/HCO3- exchange to intracellular pH (pHi) regulation in cultured chick heart cells was evaluated using ion-selective microelectrodes to monitor pHi, Na+ (aiNa), and Cl- (aiCl) activity. In (HCO3- + CO2)-buffered solution steady-state pHi was 7.12. Removing (HCO3- + CO2) buffer caused a SITS (0.1 mM)-sensitive alkalinization and countergradient increase in aiCl along with a transient DIDS-sensitive countergradient decrease in aiNa. SITS had no effect on the rate of pHi recovery from alkalinization. When (HCO3- + CO2) was reintroduced the cells rapidly acidified, aiNa incr

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30

Simchowitz, L., and A. Roos. "Regulation of intracellular pH in human neutrophils." Journal of General Physiology 85, no. 3 (1985): 443–70. http://dx.doi.org/10.1085/jgp.85.3.443.

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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

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31

Paradiso, A. M., M. C. Townsley, E. Wenzl, and T. E. Machen. "Regulation of intracellular pH in resting and in stimulated parietal cells." American Journal of Physiology-Cell Physiology 257, no. 3 (1989): C554—C561. http://dx.doi.org/10.1152/ajpcell.1989.257.3.c554.

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Microspectrofluorimetry of the pH-sensitive, fluorescent dye 2',7'-biscarboxyethyl-5 (6)-carboxyfluorescein (BCECF) was used to measure intracellular pH (pHi) in single parietal cells (PC) of intact rabbit gastric glands during resting and stimulated conditions. In 61% of PC, histamine plus isobutylmethylxanthine (IBMX) (both 100 microM) caused a small increase in pHi, ranging from 0.04 to 0.21 pH units (average delta pHi = 0.09 +/- 0.04 units over a 6-min period). In the other 39% of PC, pHi remained constant or decreased slightly (maximum decrease was 0.10 unit). The specific inhibitors omep

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32

McKinney, L. C., and A. Moran. "Regulation of intracellular pH in J774 murine macrophage cells: H+ extrusion processes." American Journal of Physiology-Cell Physiology 268, no. 1 (1995): C210—C217. http://dx.doi.org/10.1152/ajpcell.1995.268.1.c210.

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Mechanisms of intracellular pH (pHi) regulation were characterized in the murine macrophage cell line J774.1, using 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein to measure pHi. Under nominally HCO3(-)-free conditions, resting pHi of nonadherent J774.1 cells was 7.53 +/- 0.02 (n = 86), and of adherent cells was 7.59 +/- 0.02 (n = 97). In the presence of HCO3-/CO2, pHi values were reduced to 7.41 +/- 0.02 (n = 12) and 7.40 +/- 0.01 (n = 28), respectively. Amiloride, an inhibitor of Na+/H+ exchange, did not affect resting pHi. Inhibitors of a vacuolar type H(+)-ATPase [bafilomycin A1, N-ethylm

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Hosoda, Enako, Daisaku Hiraoka, Noritaka Hirohashi, Saki Omi, Takeo Kishimoto, and Kazuyoshi Chiba. "SGK regulates pH increase and cyclin B–Cdk1 activation to resume meiosis in starfish ovarian oocytes." Journal of Cell Biology 218, no. 11 (2019): 3612–29. http://dx.doi.org/10.1083/jcb.201812133.

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Tight regulation of intracellular pH (pHi) is essential for biological processes. Fully grown oocytes, having a large nucleus called the germinal vesicle, arrest at meiotic prophase I. Upon hormonal stimulus, oocytes resume meiosis to become fertilizable. At this time, the pHi increases via Na+/H+ exchanger activity, although the regulation and function of this change remain obscure. Here, we show that in starfish oocytes, serum- and glucocorticoid-regulated kinase (SGK) is activated via PI3K/TORC2/PDK1 signaling after hormonal stimulus and that SGK is required for this pHi increase and cyclin

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34

Nottingham, S., J. C. Leiter, P. Wages, S. Buhay, and J. S. Erlichman. "Developmental changes in intracellular pH regulation in medullary neurons of the rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 281, no. 6 (2001): R1940—R1951. http://dx.doi.org/10.1152/ajpregu.2001.281.6.r1940.

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We examined intracellular pH (pHi) regulation in the retrotrapezoid nucleus (RTN), a CO2-sensitive site, and the hypoglossal nucleus, a nonchemosensitive site, during development (postnatal days 2–18) in rats. Respiratory acidosis [10% CO2, extracellular pH (pHo) 7.18] caused acidification without pHi recovery in the RTN at all ages. In the hypoglossal nucleus, pHi recovered in young animals, but as animal age increased, the slope of pHi recovery diminished. In animals older than postnatal day 11, the pHi responses to hypercapnia were identical in the hypoglossal nucleus and the RTN, but hypog

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35

Hayashi, Hisayoshi, Kazuhito Suruga, and Yukari Yamashita. "Regulation of intestinal Cl−/HCO3− exchanger SLC26A3 by intracellular pH." American Journal of Physiology-Cell Physiology 296, no. 6 (2009): C1279—C1290. http://dx.doi.org/10.1152/ajpcell.00638.2008.

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SLC26A3, a Cl−/HCO3− exchanger, is highly expressed in intestinal epithelial cells, and its mutations cause congenital chloride diarrhea. This suggests that SLC26A3 plays a key role in NaCl absorption in the intestine. Electroneutral NaCl absorption in the intestine is mediated by functional coupling of the Na+/H+ exchanger and Cl−/HCO3− exchanger. It is proposed that the coupling of these exchangers may occur as a result of indirect linkage by changes of intracellular pH (pHi). We therefore investigated whether SLC26A3 is regulated by pHi. We generated a hemagglutinin epitope-tagged human SLC

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Green, J., D. T. Yamaguchi, C. R. Kleeman, and S. Muallem. "Cytosolic pH regulation in osteoblasts. Regulation of anion exchange by intracellular pH and Ca2+ ions." Journal of General Physiology 95, no. 1 (1990): 121–45. http://dx.doi.org/10.1085/jgp.95.1.121.

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Measurements of cytosolic pH (pHi) 36Cl fluxes and free cytosolic Ca2+ concentration ([Ca2+]i) were performed in the clonal osteosarcoma cell line UMR-106 to characterize the kinetic properties of Cl-/HCO3- (OH-) exchange and its regulation by pHi and [Ca2+]i. Suspending cells in Cl(-)-free medium resulted in rapid cytosolic alkalinization from pHi 7.05 to approximately 7.42. Subsequently, the cytosol acidified to pHi 7.31. Extracellular HCO3- increased the rate and extent of cytosolic alkalinization and prevented the secondary acidification. Suspending alkalinized and Cl(-)-depleted cells in

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37

Bidani, A., S. E. Brown, and T. A. Heming. "pHi regulation in alveolar macrophages: relative roles of Na(+)-H+ antiport and H(+)-ATPase." American Journal of Physiology-Lung Cellular and Molecular Physiology 266, no. 6 (1994): L681—L688. http://dx.doi.org/10.1152/ajplung.1994.266.6.l681.

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In rabbit alveolar macrophages, recovery of intracellular pH (pHi) from acid loads to pHi values > or = 6.8 at an extracellular pH (pHo) of 7.4 (nominal absence of CO2-HCO3-) is insensitive to amiloride, an inhibitor of Na(+)-H+ exchange, and abolished by bafilomycin A1, an inhibitor of vacuolar-type H(+)-ATPase [A. Bidani, S.E.S. Brown, T.A. Heming, R. Gurich, and T.D. Dubose, Jr. Am. J. Physiol. 257 (Cell Physiol. 26): C65-C76, 1989; A. Bidani and S. E. S. Brown. Am. J. Physiol. 259 (Cell Physiol. 28): C586-C598, 1990]. To further evaluate the roles of Na(+)-H+ exchange and H(+)-ATPase ac

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Akiba, Yasutada, and Jonathan D. Kaunitz. "Regulation of intracellular pH and blood flow in rat duodenal epithelium in vivo." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 1 (1999): G293—G302. http://dx.doi.org/10.1152/ajpgi.1999.276.1.g293.

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Duodenal mucosal defense was assessed by measuring blood flow and epithelial intracellular pH (pHi) of rat proximal duodenum in vivo. Fluorescence microscopy was used to measure epithelial pHi using the trapped, pHi-indicating dye 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein-AM. Blood flow was measured with laser-Doppler flowmetry. The mucosa was briefly superfused with NH4Cl, pH 2.2 buffer, the potent Na+/H+exchange inhibitor 5-( N, N-dimethyl)-amiloride (DMA), or the anion exchange and Na+-[Formula: see text]cotransport inhibitor DIDS. Cryostat sections localized dye fluorescence to the

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Coakley, Raymond J., Clifford Taggart, Noel G. McElvaney, and Shane J. O'Neill. "Cytosolic pH and the inflammatory microenvironment modulate cell death in human neutrophils after phagocytosis." Blood 100, no. 9 (2002): 3383–91. http://dx.doi.org/10.1182/blood.v100.9.3383.

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Abstract Following phagocytosis in vivo, acidification of extracellular pH (pHo) and intracellular metabolic acid generation contribute to cytosolic proton loading in neutrophils. Cytosolic pH (pHi) affects neutrophil function, although its regulation is incompletely understood. Its effect on mechanisms of neutrophil death is also uncertain. Thus, we investigated pHi regulation in Escherichia coli–exposed neutrophils, at various pathogen-to-phagocyte ratios (0:1-50:1), under conditions simulating the inflammatory milieu in vivo and correlated pHi changes with mechanisms of neutrophil death. Fo

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Piwnica-Worms, D., R. Jacob, C. R. Horres, and M. Lieberman. "Na/H exchange in cultured chick heart cells. pHi regulation." Journal of General Physiology 85, no. 1 (1985): 43–64. http://dx.doi.org/10.1085/jgp.85.1.43.

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The purpose of this study was to establish the existence of Na/H exchange in cardiac muscle and to evaluate the contribution of Na/H exchange to pHi regulation. The kinetics of pHi changes in cultured chick heart cells were monitored microfluorometrically with 6-carboxyfluorescein and correlated with Nai content changes analyzed by atomic absorption spectrophotometry; transmembrane H+ movements were evaluated under pH stat conditions. After induction of an intracellular acid load by pretreatment with NH4Cl, a regulatory cytoplasmic alkalinization occurred with a t1/2 of 2.9 min. pHi regulation

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Marshall, W. S., and S. E. Bryson. "Intracellular pH regulation in trout urinary bladder epithelium: Na(+)-H+(NH4+) exchange." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 261, no. 3 (1991): R652—R658. http://dx.doi.org/10.1152/ajpregu.1991.261.3.r652.

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We measured intracellular pH (pHi) of single epithelial cells in situ in the urinary bladder epithelium using microspectrofluorometry and the cytoplasmically trapped pH-sensitive fluorophore, 2',7'-bis(2-carboxyethyl)-5(6)- carboxyfluorescein (BCECF). The resting pHi was 7.21 +/- 0.03 (n = 40 bladders, 489 cells) in pH 7.8 bathing solutions, indicating that H+ is not passively distributed across the plasma membrane and is extruded against its electrochemical gradient. Whereas exposure to hypercapnia (5% CO2 saturation) reversibly decreased pHi, mucosally added 20 mM NH4+ reversibly increased p

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Bidani, A., and T. A. Heming. "Kinetic analysis of cytosolic pH regulation in alveolar macrophages: V-ATPase-mediated responses to a weak acid." American Journal of Physiology-Lung Cellular and Molecular Physiology 269, no. 1 (1995): L20—L29. http://dx.doi.org/10.1152/ajplung.1995.269.1.l20.

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Three different mechanisms interact to control the cytosolic pH (pHi) of alveolar macrophages (M phi), namely, plasmalemmal vacuolar-type H(+)-ATPase (V-ATPase), Na+/H+ exchange, and Na(+)-independent HCO3-/Cl- exchange. To investigate the activity of plasmalemmal V-ATPase in alveolar M phi, we developed a nonlinear mathematical model of pHi regulation that incorporates the biophysical determinants of pHi and the fluxes of individual acid-base equivalents. The model was used to analyze the acid-base responses of rabbit alveolar M phi to a weak acid (propionic acid) under conditions that favore

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Nishimura, M., D. C. Johnson, B. M. Hitzig, P. Okunieff, and H. Kazemi. "Effects of hypercapnia on brain pHi and phosphate metabolite regulation by 31P-NMR." Journal of Applied Physiology 66, no. 5 (1989): 2181–88. http://dx.doi.org/10.1152/jappl.1989.66.5.2181.

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The ability of brain cells to regulate intracellular pH (pHi) and several phosphate metabolites was evaluated during 1 h of hypercapnia (inspiratory CO2 fraction of 0.10 and 0.05) in anesthetized rats by 31P high-field (145.6 MHz) nuclear magnetic resonance spectroscopy. Body temperature was maintained at 37 +/- 0.5 degrees C. Fully relaxed spectra were obtained for controls and 30–50 min after CO2 loading and CO2 withdrawal. Spectra were taken serially every 2.5 min after gas mixtures were changed. Brain pHi decreased 0.10 +/- 0.02 units [7.06 +/- 0.01 (SE)] to 6.96 +/- 0.01 (P less than 0.00

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Helbig, H., C. Korbmacher, F. Stumpff, M. Coca-Prados, and M. Wiederholt. "Role of HCO3- in regulation of cytoplasmic pH in ciliary epithelial cells." American Journal of Physiology-Cell Physiology 257, no. 4 (1989): C696—C705. http://dx.doi.org/10.1152/ajpcell.1989.257.4.c696.

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Cytoplasmic pH (pHi) was monitored using the pH-sensitive absorbance of 5(6)carboxy-4',5'-dimethylfluorescein in monolayers of a cell clone derived from bovine pigmented ciliary epithelium (PE) transformed with the simian virus 40. 1) Changing extracellular media from a nominally HCO3(-)-free solution to a solution containing 28 mM HCO3(-)-5% CO2 at constant extracellular pH (7.4) resulted in a delayed alkalinization of pHi, which was 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) sensitive and was inhibited in Na+-free medium and in Cl(-)-depleted cells. 2) DIDS pretreatment acidifie

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Schlue, Wolf-R., and Joachim W. Deitmer. "Direct measurement of intracellular pH in identified glial cells and neurones of the leech central nervous system." Canadian Journal of Physiology and Pharmacology 65, no. 5 (1987): 978–85. http://dx.doi.org/10.1139/y87-155.

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Neutral carrier pH-sensitive double-barrelled microelectrodes were used to investigate intracellular pH (pHi) in leech neuropile glial cells and in Retzius neurones. The mean pHi of the glial cells was 6.87 ± 0.13 (± SD, n = 27) in HEPES-buffered saline (pHo 7.4) and 7.18 ± 0.19 (n = 13) in solutions buffered with 2% CO2 – 11 mM[Formula: see text]. The distribution of H+ ions in both the glia and neurones was found not to be in electrochemical equilibrium. To investigate pHi regulation, the pHi was decreased by exposure to CO2 or by adding and then removing NH4Cl. Acidification by any method w

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Nachshen, D. A., and P. Drapeau. "The regulation of cytosolic pH in isolated presynaptic nerve terminals from rat brain." Journal of General Physiology 91, no. 2 (1988): 289–303. http://dx.doi.org/10.1085/jgp.91.2.289.

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Cytosolic pH (pHi) was measured in presynaptic nerve terminals isolated from rat brain (synaptosomes) using a fluorescent pH indicator, 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF). The synaptosomes were loaded with BCECF by incubation with the membrane-permanent acetoxy-methyl ester derivative of BCECF, which is hydrolyzed by intracellular esterases to the parent compound. pHi was estimated by calibrating the fluorescence signal after permeabilizing the synaptosomal membrane by two different methods. Synaptosomes loaded with 15-90 microM BCECF were estimated to have a pHi of 6.94 +/

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47

Tonnessen, T. I., K. Sandvig, and S. Olsnes. "Role of Na(+)-H+ and Cl(-)-HCO3- antiports in the regulation of cytosolic pH near neutrality." American Journal of Physiology-Cell Physiology 258, no. 6 (1990): C1117—C1126. http://dx.doi.org/10.1152/ajpcell.1990.258.6.c1117.

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In Vero cells, Na(+)-H+ antiport as well as Na(+)-coupled and Na(+)-independent Cl(-)-HCO3- antiport are involved in regulation of cytosolic pH (pHi) after large (unphysiological) deviations from neutrality. In this paper we have studied to which extent each of the three antiports is involved in regulation of pHi after small deviations from neutrality expected to occur under physiological conditions. At physiological extracellular pH (pHo), inhibition of Na(+)-H+ exchange by amiloride did not alter pHi. At neutral and alkaline pHo, pHi was found to be lower in the presence of HCO3- than in its

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48

Portman, M. A., Y. Xiao, B. G. Broers, and X. H. Ning. "Hypoxic pHi and function modulation by Na+/H+ exchange and alpha-adrenoreceptor inhibition in heart in vivo." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 6 (1997): H2664—H2670. http://dx.doi.org/10.1152/ajpheart.1997.272.6.h2664.

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Regulation of intracellular pH (pHi) may contribute to maintenance of cardiac contractile function during graded hypoxia in vivo. To test this hypothesis, we disturbed pHi regulation in vivo using two approaches: alpha-adrenoreceptor antagonism with phentolamine (1 mg/kg) (Phen; n = 9); and Na+/H+ exchange inhibition with HOE-642 (2 mg/kg; n = 6) before graded hypoxia in open-chest sheep. Hemodynamic parameters including left ventricular maximal pressure development (dP/dtmax) cardiac index (CI), and left ventricular power were monitored continuously and simultaneously with high-energy phospha

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Milton, A. E., and I. D. Weiner. "Intracellular pH regulation in the rabbit cortical collecting duct A-type intercalated cell." American Journal of Physiology-Renal Physiology 273, no. 3 (1997): F340—F347. http://dx.doi.org/10.1152/ajprenal.1997.273.3.f340.

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The A cell may possess multiple H+ transporters, including H(+)-adenosinetriphosphatase (H(+)-ATPase) and H(+)-K(+)-ATPase. The current study examines the relative roles of proton transporters in the A cell by observing their contribution to both basal intracellular pH (pHi) regulation and pHi recovery from an intracellular acid load. CCD were studied using in vitro microperfusion, and pHi was measured in the individual A cell using the fluorescent, pH-sensitive dye, 2',7'-bis(carboxyethyl)-5(6)-carboxy-fluorescein (BCECF). Inhibiting H(+)-ATPase with luminal bafilomycin A1 decreased basal pHi

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50

Sanchez-Armass, S., R. Martinez-Zaguilan, G. M. Martinez, and R. J. Gillies. "Regulation of pH in rat brain synaptosomes. I. Role of sodium, bicarbonate, and potassium." Journal of Neurophysiology 71, no. 6 (1994): 2236–48. http://dx.doi.org/10.1152/jn.1994.71.6.2236.

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1. We investigated the regulation of intracellular pH (pHi) in rat brain isolated nerve terminals (synaptosomes), using fluorescence pH indicators and time-resolved fluorescence spectroscopy. 2. The resting pHi was not significantly affected by the presence or absence of HCO3-. Removal of external Na+, in the absence or presence of HCO3- caused a rapid acidification of pHi. The recovery from acid loads was primarily due to the activity of the Na+/H+ exchanger, confirming the relevance of this transport system in synaptosomes. 3. Our data revealed that in synaptosomes the activity of the Na+/H+

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