Journal articles on the topic 'CO2 induced pH decrease'
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1
Croxton, T. L., B. Lande, and C. A. Hirshman. "Role of intracellular pH in relaxation of porcine tracheal smooth muscle by respiratory gases." American Journal of Physiology-Lung Cellular and Molecular Physiology 268, no. 2 (February 1, 1995): L207—L213. http://dx.doi.org/10.1152/ajplung.1995.268.2.l207.
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Hypercapnia and hypoxia both relax airway smooth muscle, but the mechanisms responsible are poorly understood. Because hypercapnia and hypoxia can each decrease intracellular pH (pHi) and acidosis can inhibit Ca2+ channels, we hypothesized that decreased pHi mediates relaxation of trachealis muscle by each of these respiratory gases. To examine the relationship between pHi and tone, we measured isometric tension, bath pH, and fluorescence intensity (540 nm) in porcine tracheal smooth muscle strips loaded with 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein and excited alternately with 440- and 500-nm light. Strips equilibrated in Krebs-Henseleit solution bubbled with 95% O2-5% CO2 were contracted with carbachol and then relaxed with either 95% N2-5% CO2 or 93% O2-7% CO2. The ratio of fluorescence intensity at 500 nm to 440 nm was calibrated vs. pHi with use of nigericin. Baseline pHi was 7.19 +/- 0.03 (n = 13). Hypoxia decreased active tension by approximately 60% but did not change pHi. Hypercapnia induced decreases in tension that were associated with substantial decreases in pHi. Thus, decreased pHi does not mediate hypoxic relaxation, but the relaxation during physiologically relevant increases in CO2 concentration is associated with significant cellular acidification.
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Martoft, L., H. Stødkilde-Jørgensen, A. Forslid, H. D. Pedersen, and P. F. Jørgensen. "CO2 induced acute respiratory acidosis and brain tissue intracellular pH: a 31P NMR study in swine." Laboratory Animals 37, no. 3 (July 1, 2003): 241–48. http://dx.doi.org/10.1258/002367703766453092.
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High concentration carbon dioxide (CO2) is used to promote pre-slaughter anaesthesia in swine and poultry, as well as short-lasting surgical anaesthesia and euthanasia in laboratory animals. Questions related to animal welfare have been raised, as CO2 anaesthesia does not set in momentarily. Carbon dioxide promotes anaesthesia by lowering the intracellular pH in the brain cells, but the dynamics of the changes in response to a high concentration of CO2 is not known. Based on 31P NMR spectroscopy, we describe CO2-induced changes in intracellular pH in the brains of five pigs inhaling 90% CO2 in ambient air for a period of 60 s, and compare the results to changes in arterial blood pH, PCO2, O2 saturation and HCO3- concentration. The intracellular pH paralleled the arterial pH and PCO2 during inhalation of CO2; and it is suggested that the acute reaction to CO2 inhalation mainly reflects respiratory acidosis, and not metabolic regulation as for example transmembrane fluxes of H+/HCO3-. The intracellular pH decreased to approximately 6.7 within the 60 s inhalation period, and the situation was metabolically reversible after the end of CO2 inhalation. The fast decrease in intracellular pH supports the conclusion that high concentration CO2 leads to anaesthesia soon after the start of inhalation.
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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 (December 1, 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 increased, aiCl decreased, and pHi recovered. The decrease in aiCl and the pHi recovery were SITS sensitive. Cells exposed to 10 mM NH4Cl became transiently alkaline concomitant with an increase in aiCl and a decrease in aiNa. The intracellular acidification induced by NH4Cl removal was accompanied by a decrease in aiCl and an increase in aiNa that led to the recovery of pHi. In the presence of (HCO3- + CO2), addition of either amiloride (1 mM) or DIDS (1 mM) partially reduced pHi recovery, whereas application of amiloride plus DIDS completely inhibited the pHi recovery and the decrease in aiCl. Therefore, after an acid load pHi recovery is HCO3o- and Nao- dependent and DIDS sensitive (but not Ca2+o dependent). Furthermore, SITS inhibition of Na(+)-dependent Cl-/HCO3- exchange caused an increase in aiCl and a decrease in the 36Cl efflux rate constant and pHi. In (HCO3- + CO2)-free solution, amiloride completely blocked the pHi recovery from acidification that was induced by removal of NH4Cl. Thus, both Na+/H+ and Na(+)-dependent Cl-/HCO3- exchange are involved in pHi regulation from acidification. When the cells became alkaline upon removal of (HCO3- + CO2), a SITS-sensitive increase in pHi and aiCl was accompanied by a decrease of aiNa, suggesting that the HCO3- efflux, which can attenuate initial alkalinization, is via a Na(+)-dependent Cl-/HCO3- exchange. However, the mechanism involved in pHi regulation from alkalinization is yet to be established. In conclusion, in cultured chick heart cells the Na(+)-dependent Cl-/HCO3- exchange regulates pHi response to acidification and is involved in the steady-state maintenance of pHi.
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Preibisch, Imke, Lena-Marie Ränger, Pavel Gurikov, and Irina Smirnova. "In Situ Measurement Methods for the CO2-Induced Gelation of Biopolymer Systems." Gels 6, no. 3 (September 9, 2020): 28. http://dx.doi.org/10.3390/gels6030028.
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This work presents two novel methods to investigate in situ the carbon dioxide (CO2)-induced gelation of biopolymer-based solutions. The CO2-induced gelation is performed in a viewing cell at room temperature under CO2 pressure (20 to 60 bar), whereby calcium precursors are used as cross-linkers. The novel methods allow the in situ optical observation and evaluation of the gelation process via the change in turbidity due to dissolution of dispersed calcium carbonate (CaCO3) particles and in situ pH measurements. The combination of both methods enables the determination of the gelation direction, gelation rate, and the pH value in spatial and temporal resolution. The optical gelation front and pH front both propagate equally from top to bottom through the sample solutions, indicating a direct link between a decrease in the pH value and the dissolution of the CaCO3 particles. Close-to-vertical movement of both gelation front and pH front suggests almost one dimensional diffusion of CO2 from the contact surface (gel–CO2) to the bottom of the sample. The gelation rate increases with the increase in CO2 pressure. However, the increase in solution viscosity and the formation of a gel layer result in a strong decrease in the gelation rate due to a hindrance of CO2 diffusion. Released carbonate ions from CaCO3 dissolution directly influence the reaction equilibrium between CO2 and water and therefore the change in pH value of the solution. Increasing the CaCO3 concentrations up to the solubility results in lower gelation rates.
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Lyall, Vijay, Rammy I. Alam, Tam-Hao T. Phan, Oneal F. Russell, Shahbaz A. Malik, Gerard L. Heck, and John A. DeSimone. "Modulation of Rat Chorda Tympani NaCl Responses and Intracellular Na+ Activity in Polarized Taste Receptor Cells by pH." Journal of General Physiology 120, no. 6 (November 25, 2002): 793–815. http://dx.doi.org/10.1085/jgp.20028656.
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Mixture interactions between sour and salt taste modalities were investigated in rats by direct measurement of intracellular pH (pHi) and Na+ activity ([Na+]i) in polarized fungiform taste receptor cells (TRCs) and by chorda tympani (CT) nerve recordings. Stimulating the lingual surface with NaCl solutions adjusted to pHs ranging between 2.0 and 10.3 increased the magnitude of NaCl CT responses linearly with increasing external pH (pHo). At pH 7.0, the epithelial sodium channel (ENaC) blocker, benzamil, decreased NaCl CT responses and inhibited further changes in CT responses induced by varying pHo to 2.0 or 10.3. At constant pHo, buffering NaCl solutions with potassium acetate/acetic acid (KA/AA) or HCO3−/CO2 inhibited NaCl CT responses relative to CT responses obtained with NaCl solutions buffered with HEPES. The carbonic anhydrase blockers, MK-507 and MK-417, attenuated the inhibition of NaCl CT responses in HCO3−/CO2 buffer, suggesting a regulatory role for pHi. In polarized TRCs step changes in apical pHo from 10.3 to 2.0 induced a linear decrease in pHi that remained within the physiological range (slope = 0.035; r2 = 0.98). At constant pHo, perfusing the apical membrane with Ringer's solutions buffered with KA/AA or HCO3−/CO2 decreased resting TRC pHi, and MK-507 or MK-417 attenuated the decrease in pHi in TRCs perfused with HCO3−/CO2 buffer. In parallel experiments, TRC [Na+]i decreased with (a) a decrease in apical pH, (b) exposing the apical membrane to amiloride or benzamil, (c) removal of apical Na+, and (d) acid loading the cells with NH4Cl or sodium acetate at constant pHo. Diethylpyrocarbonate and Zn2+, modification reagents for histidine residues in proteins, attenuated the CO2-induced inhibition of NaCl CT responses and the pHi-induced inhibition of apical Na+ influx in TRCs. We conclude that TRC pHi regulates Na+-influx through amiloride-sensitive apical ENaCs and hence modulates NaCl CT responses in acid/salt mixtures.
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Nero, A. C., J. H. Schwartz, and M. R. Furtado. "Characteristics of H+ current transients induced by adverse H+ gradient pulses in toad bladder." American Journal of Physiology-Renal Physiology 253, no. 4 (October 1, 1987): F606—F612. http://dx.doi.org/10.1152/ajprenal.1987.253.4.f606.
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Acidification in the toad bladder occurs as a result of electrogenic H+ secretion (JH). When a pH gradient is applied in a stepwise fashion in the absence of exogenous CO2, JH decreases linearly with the mucosal (M) solution pH and is null when pHm is approximately 4.5. When pHm is returned to initial values (7.4) in a stepwise fashion, JH increases linearly with pHm. However, on this return, higher values of JH are initially obtained. To investigate this hysteresis, hemibladders mounted in chambers were used to measure the change in the H+ current before and after acid pulses were applied to the mucosal solution. In the absence of exogenous CO2, the application of graded acid pulses to mucosa for 1, 2, 4, and 8 min resulted in a graded decrease in JH. The restoration of pHm to 7.4 was followed by an immediate transient overshoot of reversed short-circuit current (Irsc), which was related to the time of exposure and the magnitude of the acid pulse. The longer the acid pulse or the larger the pulse, the greater the Irsc overshoot. The addition of protonophores, dinitrophenol, or salicylate, into the mucosal solution enhanced this overshoot. Similar Irsc overshoots could be obtained with the application of pulses of adverse electrical gradients. Introduction of exogenous CO2 into the system (3%) completely inhibited the overshoot in JH after an acid pulse. In conclusion, when pHm is decreased JH is reduced and the cell pH presumably decreases because of continued exit of alkali at the serosal side of the cell and entry of H+ from the mucosal solution. The decrease in cell pH then triggers the pump to produce a sharp overshoot in JH when pHm returns to 7.4.
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Lyall, Vijay, Hampton Pasley, Tam-Hao T. Phan, Shobha Mummalaneni, Gerard L. Heck, Anna K. Vinnikova, and John A. DeSimone. "Intracellular pH Modulates Taste Receptor Cell Volume and the Phasic Part of the Chorda Tympani Response to Acids." Journal of General Physiology 127, no. 1 (December 27, 2005): 15–34. http://dx.doi.org/10.1085/jgp.200509384.
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The relationship between cell volume and the neural response to acidic stimuli was investigated by simultaneous measurements of intracellular pH (pHi) and cell volume in polarized fungiform taste receptor cells (TRCs) using 2',7'-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein (BCECF) in vitro and by rat chorda tympani (CT) nerve recordings in vivo. CT responses to HCl and CO2 were recorded in the presence of 1 M mannitol and specific probes for filamentous (F) actin (phalloidin) and monomeric (G) actin (cytochalasin B) under lingual voltage clamp. Acidic stimuli reversibly decrease TRC pHi and cell volume. In isolated TRCs F-actin and G-actin were labeled with rhodamine phalloidin and bovine pancreatic deoxyribonuclease-1 conjugated with Alexa Fluor 488, respectively. A decrease in pHi shifted the equilibrium from F-actin to G-actin. Treatment with phalloidin or cytochalasin B attenuated the magnitude of the pHi-induced decrease in TRC volume. The phasic part of the CT response to HCl or CO2 was significantly decreased by preshrinking TRCs with hypertonic mannitol and lingual application of 1.2 mM phalloidin or 20 μM cytochalasin B with no effect on the tonic part of the CT response. In TRCs first treated with cytochalasin B, the decrease in the magnitude of the phasic response to acidic stimuli was reversed by phalloidin treatment. The pHi-induced decrease in TRC volume induced a flufenamic acid–sensitive nonselective basolateral cation conductance. Channel activity was enhanced at positive lingual clamp voltages. Lingual application of flufenamic acid decreased the magnitude of the phasic part of the CT response to HCl and CO2. Flufenamic acid and hypertonic mannitol were additive in inhibiting the phasic response. We conclude that a decrease in pHi induces TRC shrinkage through its effect on the actin cytoskeleton and activates a flufenamic acid–sensitive basolateral cation conductance that is involved in eliciting the phasic part of the CT response to acidic stimuli.
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Offner, B., J. Czachurski, S. A. Konig, and H. Seller. "Different effects of respiratory and metabolic acidosis on preganglionic sympathetic nerve activity." Journal of Applied Physiology 77, no. 1 (July 1, 1994): 173–78. http://dx.doi.org/10.1152/jappl.1994.77.1.173.
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We studied sympathetic nerve activity (SNA) responses, recorded in multifiber preparations of left third thoracic white ramus, to respiratory or isocapnic metabolic acidosis or to CO2 enhancement at constant pH in chloralose-anesthetized paralyzed artificially ventilated cats. Cardiopulmonary, baro-, and peripheral chemoreceptors were denervated by bilaterally cutting vagus and carotid sinus nerves. Acidosis was induced by either decreasing artificial ventilation or infusing HCl (0.5 M i.v.). Both respiratory and isocapnic metabolic acidosis induced a decrease in local extracellular pH, measured directly with pH-sensitive microelectrodes within medulla region containing sympathoexcitatory bulbospinal neurons. The magnitude of changes in medullary pH was independent of the way systemic acidosis was generated. Despite uniformity of changes in local medullary extracellular pH due to systemic respiratory or isocapnic metabolic acidosis, different responses were observed in preganglionic SNA. Isocapnic metabolic acidosis resulted in a slight increase in SNA, averaging 6.4% per 0.05 systemic pH unit decrease. In contrast, respiratory acidosis induced by decreasing artificial ventilation produced a more pronounced increase of SNA, reaching peak changes of approximately 70% compared with control level with normal blood gases, an average increase of 13% per 0.05 systemic pH unit decrease. We conclude that systemic CO2 and H+ concentrations represent different stimuli to sympathetic nervous system. Despite similar changes of local extracellular pH within rostral ventrolateral medulla during systemic acidosis, different responses of SNA suggest other sites or as yet unknown additional effects of CO2 as being responsible for excitation of sympathetic activity.
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Rassier, Dilson E., and Walter Herzog. "Effects of pH on the length-dependent twitch potentiation in skeletal muscle." Journal of Applied Physiology 92, no. 3 (March 1, 2002): 1293–99. http://dx.doi.org/10.1152/japplphysiol.00912.2001.
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When muscle is elongated, there is a length dependence of twitch potentiation and an increased Ca2+ sensitivity of the myofilaments. Changes in the charge potential of myofilaments, induced by a decrease in pH, are known to abolish the length dependence of Ca2+ sensitivity. This study was aimed at testing the hypothesis that a decrease in pH, and the concomitant loss of length dependence of Ca2+sensitivity, depresses the length dependence of staircase potentiation. In vitro, isometric twitch contractions of fiber bundles dissected from the mouse extensor digitorum longus, performed before and after 10 s of 10-Hz stimulation (i.e., the staircase potentiation protocol) were analyzed at five different lengths, ranging from optimal length for maximal force production ( L o; = 12 ± 0.7 mm) to L o + 1.2 mm ( L o + 10%). These measurements were made at an extracellular pH of 6.6, 7.4, and 7.8 (pH changes induced by altering the CO2 concentration of the bath solution). At pH 7.4 and 7.8, the degree of potentiation after 10-Hz stimulation showed a linear decrease with increased fiber bundle length ( r 2 = 0.95 and r 2 = 0.99, respectively). At pH 6.6, the length dependence of potentiation was abolished, and the slope of the length-potentiation relationship was not different from zero ( r 2 = 0.05). The results of this study indicate that length dependence of potentiation in intact skeletal muscle is abolished by lowering the pH. Because decreasing the pH decreases Ca2+ sensitivity and changes the charge potential of the filaments, the mechanism of length-dependent potentiation may be closely related to the length dependence of Ca2+sensitivity, and changes in the charge potential of the myofilaments may be important in regulating this relationship.
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Sganga, Daniela E., Flemming T. Dahlke, Sune R. Sørensen, Ian A. E. Butts, Jonna Tomkiewicz, David Mazurais, Arianna Servili, Francesca Bertolini, and Sebastian N. Politis. "CO2 induced seawater acidification impacts survival and development of European eel embryos." PLOS ONE 17, no. 4 (April 18, 2022): e0267228. http://dx.doi.org/10.1371/journal.pone.0267228.
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Fish embryos may be vulnerable to seawater acidification resulting from anthropogenic carbon dioxide (CO2) emissions or from excessive biological CO2 production in aquaculture systems. This study investigated CO2 effects on embryos of the European eel (Anguilla anguilla), a catadromous fish that is considered at risk from climate change and that is targeted for hatchery production to sustain aquaculture of the species. Eel embryos were reared in three independent recirculation systems with different pH/CO2 levels representing “control” (pH 8.1, 300 μatm CO2), end-of-century climate change (“intermediate”, pH 7.6, 900 μatm CO2) and “extreme” aquaculture conditions (pH 7.1, 3000 μatm CO2). Sensitivity analyses were conducted at 4, 24, and 48 hours post-fertilization (hpf) by focusing on development, survival, and expression of genes related to acute stress response (crhr1, crfr2), stress/repair response (hsp70, hsp90), water and solute transport (aqp1, aqp3), acid-base regulation (nkcc1a, ncc, car15), and inhibitory neurotransmission (GABAAα6b, Gabra1). Results revealed that embryos developing at intermediate pH showed similar survival rates to the control, but egg swelling was impaired, resulting in a reduction in egg size with decreasing pH. Embryos exposed to extreme pH had 0.6-fold decrease in survival at 24 hpf and a 0.3-fold change at 48 compared to the control. These observed effects of acidification were not reflected by changes in expression of any of the here studied genes. On the contrary, differential expression was observed along embryonic development independent of treatment, indicating that the underlying regulating systems are under development and that embryos are limited in their ability to regulate molecular responses to acidification. In conclusion, exposure to predicted end-of-century ocean pCO2 conditions may affect normal development of this species in nature during sensitive early life history stages with limited physiological response capacities, while extreme acidification will negatively influence embryonic survival and development under hatchery conditions.
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van Adelsberg, J., and Q. Al-Awqati. "Regulation of cell pH by Ca+2-mediated exocytotic insertion of H+-ATPases." Journal of Cell Biology 102, no. 5 (May 1, 1986): 1638–45. http://dx.doi.org/10.1083/jcb.102.5.1638.
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Exposure to CO2 acidifies the cytosol of mitochondria-rich cells in turtle bladder epithelium. The result of the decrease in pH in these, the acid-secreting cells of the epithelium, is a transient increase in cell calcium, which causes exocytosis of vesicles containing proton-translocating ATPase. Because mitochondria-rich cells have rapid luminal membrane turnover, we were able to identify single mitochondria-rich cells by their endocytosis of rhodamine-tagged albumin. Using fluorescence emission of 5,6-carboxyfluorescein at two excitation wavelengths, we measured cell pH in these identified mitochondria-rich cells and found that although the cell pH fell, it recovered within 5 min despite continuous exposure to CO2. This pH recovery also occurred at the same rate in Na+-free media. However, pH recovery did not occur when luminal pH was 5.5, a condition under which the H+-pump does not function, suggesting that recovery of cell pH is due to the luminally located H+ ATPase. Chelation of extracellular calcium by EGTA prevented the CO2-induced rise in cell calcium measured with the intracellular fluorescent dyes Quin 2 or Fura 2 and also prevented recovery of cell pH. When the change in cell calcium was buffered by loading the cells with high concentrations of Quin 2, the CO2-induced decrease in pH did not return back to basal levels. We had found previously that buffering intracellular calcium transients prevented CO2-stimulated exocytosis. Further, we show here that the increased H+ current in voltage-clamped turtle bladders, which is directly proportional to the number of H+-pump-containing vesicles that fuse with the luminal membrane, was significantly reduced in calcium-depleted bladders. These results suggest that pH regulation in these acid-secreting cells occurs by calcium-dependent exocytosis of vesicles containing proton pumps, whose subsequent turnover restores the cell pH to its initial levels.
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Lang, Carol J., Ping Dong, Emma K. Hosszu, and Ian R. Doyle. "Effect of CO2 on LPS-induced cytokine responses in rat alveolar macrophages." American Journal of Physiology-Lung Cellular and Molecular Physiology 289, no. 1 (July 2005): L96—L103. http://dx.doi.org/10.1152/ajplung.00394.2004.
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Alveolar macrophages (AM) may be exposed to a range of CO2 and pH levels depending on their location in the alveoli and the health of the lung. Cytokines produced by AM contribute to inflammation in acute lung injury (ALI). Current ventilatory practices for the management of ALI favor low tidal volumes, which can give rise to increases in CO2 and changes in pH of the alveolar microenvironment. Here we examined the effect of CO2 on cytokine release from LPS-stimulated rat AM. AM were incubated for 1–4 h under different atmospheric gas mixtures ranging from 2.5–20% CO2. To distinguish between effects of pH and CO2, the culture media were also buffered to pH 7.2 with NaHCO3. Cell metabolic activity, but not cell viability, decreased and increased significantly after 4 h at 20 and 2.5% CO2, respectively. Increasing CO2 decreased TNF-α secretion but had no effect on lysate TNF-α. Buffering the media abated the effects of CO2 on TNF-α secretion. CO2 increased cytokine-induced neutrophil chemoattractant factor-1 secretion only when the pH was buffered to 7.2. Effects of CO2 on cytokine responses were reversible. In conclusion, the effects of CO2 on cytokine lysate levels and/or secretion in AM are cytokine specific and, depending on both the cytokine and the immediate microenvironment, may be beneficial or detrimental to ALI.
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Harrison, S. M., J. E. Frampton, E. McCall, M. R. Boyett, and C. H. Orchard. "Contraction and intracellular Ca2+, Na+, and H+ during acidosis in rat ventricular myocytes." American Journal of Physiology-Cell Physiology 262, no. 2 (February 1, 1992): C348—C357. http://dx.doi.org/10.1152/ajpcell.1992.262.2.c348.
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We have investigated the effect of a CO2-induced (respiratory) acidosis on contraction and on intracellular Ca2+, Na+, and pH (measured using the fluorescent dyes fura-2, sodium-binding benzofuran isophthalate, and 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein, respectively) in ventricular myocytes isolated from rat hearts. Initial exposure to acidosis led to a rapid decrease in intracellular pH that was accompanied by an abrupt decline in contractility. There were no consistent changes of intracellular Na+ or Ca2+ during this period. The rapid decline of contractility was followed by a slower partial recovery, which was accompanied by increases in intracellular Na+, systolic and diastolic Ca2+, and an increase in the Ca2+ content of the sarcoplasmic reticulum (estimated using caffeine). Intracellular pH did not change during this slow recovery. The slow rise of intracellular Na+ and the recovery of the twitch were blocked by the Na(+)-H+ exchange inhibitor amiloride. The sarcoplasmic reticulum inhibitor ryanodine blocked the recovery of the twitch but had no effect on the rise of intracellular Na+ induced during acidosis. It is concluded that a major cause of the initial decline of the twitch during acidosis is a decrease in the response of the contractile proteins to Ca2+ due to the decrease of intracellular pH. The subsequent slow recovery of the twitch is due to the decrease of intracellular pH activating the Na(+)-H+ exchange mechanism. This elevates intracellular Na+ and presumably, via the Na(+)-Ca2+ exchange mechanism, intracellular Ca2+. This in turn may lead to increased Ca2+ loading of, and hence release from, the sarcoplasmic reticulum, and it is this that underlies the partial recovery of contraction during acidosis in this preparation.
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Gorter, Karin A. M., Marco C. Stehouwer, Bart P. Van Putte, Eline A. Vlot, and Rolf T. Urbanus. "Acidosis induced by carbon dioxide insufflation decreases heparin potency: a risk factor for thrombus formation." Perfusion 32, no. 3 (October 27, 2016): 214–19. http://dx.doi.org/10.1177/0267659116677307.
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Background: Since the introduction of CO2 insufflation during open heart surgery in our hospital, we incidentally observed thrombus formation in the dissected heart, in the pericardium and in the cardiotomy reservoir of the cardiopulmonary bypass system. Furthermore, we measured very high levels of pCO2, causing severe acidosis, in stagnant blood in the pericardium and cardiotomy reservoir. Objectives: In this in vitro study, we assessed the influence of acidosis and hypothermia on heparin potency and thrombin formation. Methods: We assessed heparin potency in function of pH (pH 5.0-7.4) and temperature (24-37°C) by comparing the activated partial thromboplastin time in platelet-poor plasma between samples with and without unfractionated heparin. We measured thrombin formation in platelet-poor plasma by means of fluorescent, calibrated, automated thrombography in function of pH (pH 5.0-7.4) and temperature (24-37°C). The parameters of interest were the endogenous thrombin potential and the peak amount of thrombin generation. Results: The major finding of this study is the significant decrease in the efficiency of unfractionated heparin in delaying thrombus formation at acidotic (pH 5.0-7.0) conditions (p=0.034-0.05). Furthermore, we found that thrombin formation is significantly increased at hypothermic (24-34°C) conditions (p=<0.001-0.01). Conclusions: Based on the results of our in-vitro study, we conclude that acidosis may lead to a decreased heparin potency. Acidosis, as induced by CO2 insufflation, may predispose patients to incidental thrombus formation in stagnant blood in the open thorax and in the cardiotomy reservoir. Hypothermia might further increase this risk. Therefore, we recommend reconsidering the potential advantages and disadvantages of using CO2 insufflation during cardiopulmonary bypass.
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Burtin, B., and J. C. Massabuau. "Switch from Metabolic to Ventilatory Compensation of Extracellular pH in Crayfish." Journal of Experimental Biology 137, no. 1 (July 1, 1988): 411–20. http://dx.doi.org/10.1242/jeb.137.1.411.
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The mechanisms of extracellular pH regulation were studied in crayfish Astacus leptodactylus under conditions that were either favourable or unfavourable for ionoregulation. Animals in intermoult or premoult stages were kept in normoxic artificial waters at 13°C. In intermoult, acid—base balance (ABB) and ionoregulatory disturbances were induced by increasing the ambient partial pressure of CO2 (PwCOCO2), by decreasing the concentration of NaCl in the water ([NaCl]w) or by associating both changes. In premoult we took advantage of the spontaneously occurring endogenous problems of ionoregulation which are linked to shell shedding. In intermoult, an increase of PwCOCO2 alone induced a hypercapnic acidosis compensated by metabolic means, whereas in association with a decrease of [NaCl]w (which induced a decrease of [NaCl] in the haemolymph) it led to a ventilatory compensation. In intermoult a decrease of [NaCl]w alone induced a metabolic acidosis that was compensated by metabolic means, whereas in premoult it was compensated by ventilatory adjustments. It is concluded that when water breathers are facing experimentally induced or spontaneous ionoregulatory problems, compensation for superimposed ABB disturbances can be made by ventilatory adjustments instead of by metabolic means.
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Krapf, R., R. J. Alpern, F. C. Rector, and C. A. Berry. "Basolateral membrane Na/base cotransport is dependent on CO2/HCO3 in the proximal convoluted tubule." Journal of General Physiology 90, no. 6 (December 1, 1987): 833–53. http://dx.doi.org/10.1085/jgp.90.6.833.
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The mechanism of basolateral membrane base transport was examined in the in vitro microperfused rabbit proximal convoluted tubule (PCT) in the absence and presence of ambient CO2/HCO3- by means of the microfluorometric measurement of cell pH. The buffer capacity of the cells measured using rapid NH3 washout was 42.8 +/- 5.6 mmol.liter-1.pH unit-1 in the absence and 84.6 +/- 7.3 mmol.liter-1.pH unit-1 in the presence of CO2/HCO3-. In the presence of CO2/HCO3-, lowering peritubular pH from 7.4 to 6.8 acidified the cell by 0.30 pH units and lowering peritubular Na from 147 to 0 mM acidified the cell by 0.25 pH units. Both effects were inhibited by peritubular 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonate (SITS). In the absence of exogenous CO2/HCO3-, lowering peritubular pH from 7.4 to 6.8 acidified the cell by 0.25 pH units and lowering peritubular Na from 147 to 0 mM decreased cell pH by 0.20 pH units. Lowering bath pH from 7.4 to 6.8 induced a proton flux of 643 +/- 51 pmol.mm-1.min-1 in the presence of exogenous CO2/HCO3- and 223 +/- 27 pmol.mm-1.min-1 in its absence. Lowering bath Na from 147 to 0 mM induced proton fluxes of 596 +/- 77 pmol.mm-1.min-1 in its absence. The cell acidification induced by lowering bath pH or bath Na in the absence of CO2/HCO3- was inhibited by peritubular SITS or by acetazolamide, whereas peritubular amiloride had no effect. In the absence of exogenous CO2/HCO3-, cyanide blocked the cell acidification induced by bath Na removal, but was without effect in the presence of exogenous CO2/HCO3-. We reached the following conclusions. (a) The basolateral Na/base n greater than 1 cotransporter in the rabbit PCT has an absolute requirement for CO2/HCO3-. (b) In spite of this CO2 dependence, in the absence of exogenous CO2/HCO3-, metabolically produced CO2/HCO3- is sufficient to keep the transporter running at 30% of its control rate in the presence of ambient CO2/HCO3-. (c) There is no apparent amiloride-sensitive Na/H antiporter on the basolateral membrane of the rabbit PCT.
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Adijanto, Jeffrey, Tina Banzon, Stephen Jalickee, Nam S. Wang, and Sheldon S. Miller. "CO2-induced ion and fluid transport in human retinal pigment epithelium." Journal of General Physiology 133, no. 6 (May 25, 2009): 603–22. http://dx.doi.org/10.1085/jgp.200810169.
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In the intact eye, the transition from light to dark alters pH, [Ca2+], and [K] in the subretinal space (SRS) separating the photoreceptor outer segments and the apical membrane of the retinal pigment epithelium (RPE). In addition to these changes, oxygen consumption in the retina increases with a concomitant release of CO2 and H2O into the SRS. The RPE maintains SRS pH and volume homeostasis by transporting these metabolic byproducts to the choroidal blood supply. In vitro, we mimicked the transition from light to dark by increasing apical bath CO2 from 5 to 13%; this maneuver decreased cell pH from 7.37 ± 0.05 to 7.14 ± 0.06 (n = 13). Our analysis of native and cultured fetal human RPE shows that the apical membrane is significantly more permeable (≈10-fold; n = 7) to CO2 than the basolateral membrane, perhaps due to its larger exposed surface area. The limited CO2 diffusion at the basolateral membrane promotes carbonic anhydrase–mediated HCO3 transport by a basolateral membrane Na/nHCO3 cotransporter. The activity of this transporter was increased by elevating apical bath CO2 and was reduced by dorzolamide. Increasing apical bath CO2 also increased intracellular Na from 15.7 ± 3.3 to 24.0 ± 5.3 mM (n = 6; P < 0.05) by increasing apical membrane Na uptake. The CO2-induced acidification also inhibited the basolateral membrane Cl/HCO3 exchanger and increased net steady-state fluid absorption from 2.8 ± 1.6 to 6.7 ± 2.3 µl × cm−2 × hr−1 (n = 5; P < 0.05). The present experiments show how the RPE can accommodate the increased retinal production of CO2 and H2O in the dark, thus preventing acidosis in the SRS. This homeostatic process would preserve the close anatomical relationship between photoreceptor outer segments and RPE in the dark and light, thus protecting the health of the photoreceptors.
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Malan, A. "pH and hypometabolism in mammalian hibernation." Canadian Journal of Zoology 66, no. 1 (January 1, 1988): 95–98. http://dx.doi.org/10.1139/z88-013.
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In mammalian hibernation, the reduction of metabolic rate occurs by three processes: inhibition of cold-induced thermogenesis, temperature effect on metabolic reaction rates (Q10), and a further inhibition. Concomitantly, the animal undergoes a marked respiratory acidosis (CO2 retention). At the intracellular level, a respiratory acidosis occurs in brain and muscles, suggesting that intracellular pH regulation is depressed. The hyperventilation of early arousal provides evidence for the hypothesis that acidosis exerts an inhibition in hibernation, and should be removed to permit thermogenesis. Muscle glycolysis and brown adipose tissue thermogenesis are depressed by acidosis in vitro, but a decrease in pH probably also affects other systems, especially the preoptic area of the hypothalamus.
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Yamakage, M., K. S. Lindeman, C. A. Hirshman, and T. L. Croxton. "Intracellular pH regulates voltage-dependent Ca2+ channels in porcine tracheal smooth muscle cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 268, no. 4 (April 1, 1995): L642—L646. http://dx.doi.org/10.1152/ajplung.1995.268.4.l642.
Full textAbstract:
Changes in CO2 or in pH modify airway smooth muscle contractility. To investigate the mechanisms involved, we compared K(+)-induced contractions in porcine bronchial rings exposed to different CO2 concentrations and directly measured the effects of changes in intracellular (pHi) or extracellular pH (pHo) on Ca2+ currents (ICa) through voltage-dependent Ca2+ channels (VDC) in porcine tracheal smooth muscle cells. Hypocapnia and hypercapnia caused leftward and rightward shifts, respectively, in the dose-response to K+ (P < 0.05) but did not change the maximum force obtained. Peak ICa (10 mM external Ca2+) elicited by depolarizing pulses from -80 mV was maximal [-265 +/- 12 pA (mean +/- SE), n = 19] at +10 mV. Intracellular acidification decreased the peak ICa at +10 mV from -261 +/- 20 pA to -177 +/- 12 pA (P < 0.05, n = 4), while intracellular alkalinization increased the peak ICa at +10 mV from -302 +/- 27 pA to -368 +/- 26 pA (P < 0.05, n = 4). Changes in pHo had little effect on ICa. There was no shift in the voltage-dependence of induced ICa with any change. We conclude that pHi, but not pHo, directly modulates the entry of Ca2+ into airway smooth muscle cells through VDC. This mechanism may contribute to regulation of airway tone by CO2.
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Tojima, H., T. Kuriyama, and Y. Fukuda. "Differential respiratory effects of HCO3- and CO2 applied on ventral medullary surface of rats." Journal of Applied Physiology 70, no. 5 (May 1, 1991): 2217–25. http://dx.doi.org/10.1152/jappl.1991.70.5.2217.
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To estimate whether H+ is the unique stimulus of the medullary chemosensor, ventilatory effects of HCO3- and/or CO2 applied on the ventral medullary surface using an improved superfusion technique and of CO2 inhalation were compared in halothane-anesthetized spontaneously breathing rats. Superfusion with low [HCO3-]-acid mock cerebrospinal fluid (CSF) (normal Pco2) induced a significant increase in ventilation, with an accompanying reduction in endtidal Pco2 (PETco2). High [HCO3-]-alkaline CSF depressed ventilation. Changes in Pco2 of superfusing CSF, on the other hand, had no significant effect despite the similar changes in pH. Simultaneous decrease in [HCO3-] and Pco2 of mock CSF with normal pH also maintained stimulated respiration. CO2 inhalation during superfusion with various [HCO3-] solutions caused further increase in ventilation as PETco2 increased. The results suggest that the surface area of the rat ventral medulla contains HCO3- (or H+)-sensitive respiratory neural substrates which are, however, little affected by CO2 in the subarachnoid fluid. A CO2 (or CO2-induced H+)-sensitive chemosensor responsible for the increase in ventilation during CO2 inhalation may exist elsewhere functionally apart from the HCO3- (or H+)-sensitive sensor in the examined surface area.
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Hsu, P., M. L. Albuquerque, and C. W. Leffler. "Mechanisms of hypercapnia-stimulated PG production in piglet cerebral microvascular endothelial cells." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 2 (February 1, 1995): H591—H603. http://dx.doi.org/10.1152/ajpheart.1995.268.2.h591.
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High CO2 stimulates dilator prostanoid (prostaglandin; PG) synthesis by piglet cerebral microvascular endothelial cells, but the mechanism of stimulation is unclear. We address the hypothesis that intracellular pH (pHi) and Ca2+ signaling are involved. When extracellular pH (pHe) and PCO2 were constant and pHi was rapidly reduced (propionate or nigericin), PG synthesis was stimulated. When pHe was lowered by reducing NaHCO3, pHi fell slowly, but PG synthesis was not altered. When pHe was decreased by increasing PCO2 or returned to 7.4 by increasing NaHCO3, with a constant PCO2 of 100 mmHg, pHi dropped quickly and PG synthesis was stimulated. When pHi was reduced slowly by changing CO2 slowly, or by stepwise addition of propionate, PG synthesis was increased regardless of pHe, suggesting that the rapid decline of pHi plays a central role in mediating the PG synthesis. Ca2+ signaling is a potential mechanism by which pHi increases PG synthesis. However, extracellular Ca2+ removal did not affect PG synthesis induced by propionate or hypercapnia. Furthermore, neither rapid nor slow decreases of pHi altered cytosolic free Ca2+ concentration. Therefore, Ca2+ signals do not appear to be involved in the CO2 stimulation of PG synthesis.
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Yu, H., and J. Ferrier. "Osteoclast ATP receptor activation leads to a transient decrease in intracellular pH." Journal of Cell Science 108, no. 9 (September 1, 1995): 3051–58. http://dx.doi.org/10.1242/jcs.108.9.3051.
Full textAbstract:
Application of extracellular adenosine triphosphate (ATP) induces a pulsed decrease in osteoclast intracellular pH (pHi), as measured with seminaphthofluorescein (SNAFL)-calcein on a laser scanning confocal microscope. Adenosine diphosphate also produces a pHi decrease, but adenosine monophosphate, uridine triphosphate, 2-methylthio-ATP, and beta, gamma-methylene-ATP have little effect on pHi. The ATP-induced pHi decrease is largely inhibited by suramin, a P2 purinergic receptor blocker. Clamping intracellular free [Ca2+] ([Ca2+]i) with BAPTA/AM does not affect the ATP-induced pHi change, showing that this pHi decrease is not caused by the increased intracellular [Ca2+]i that is produced by activation of osteoclast purinergic receptors. We show that an increase in [Ca2+]i by itself will produce a pHi increase. The ATP effect is not blocked by inhibition of Na+/H+ exchange by either Na(+)-free bathing medium or amiloride. Two inhibitors of the osteoclast cell membrane proton pump, N-ethylmaleimide and vanadate, produce partial inhibition of the ATP-induced pHi decrease. Two other proton pump inhibitors, bafilomycin and N,N'-dicyclohexylcarbodiimide, have no influence on the ATP effect. None of the proton pump inhibitors but vanadate has a direct effect on pHi. Vanadate produces a transient pHi increase upon application to the bathing medium, possibly as a result of its known effect of stimulating the Na+/H+ exchanger. Inhibition of Cl-/HCO3- exchange by decreasing extracellular Cl- gives a pronounced long-term pHi increase, supporting the hypothesis that this exchange has an important role in osteoclast pHi homeostasis. In Cl(-)-free extracellular medium, there is a greatly reduced effect of extracellular ATP on pHi.(ABSTRACT TRUNCATED AT 250 WORDS)
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Serrano, C. V., A. Fraticelli, R. Paniccia, A. Teti, B. Noble, S. Corda, T. Faraggiana, R. C. Ziegelstein, J. L. Zweier, and M. C. Capogrossi. "pH dependence of neutrophil-endothelial cell adhesion and adhesion molecule expression." American Journal of Physiology-Cell Physiology 271, no. 3 (September 1, 1996): C962—C970. http://dx.doi.org/10.1152/ajpcell.1996.271.3.c962.
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Neutrophil adhesion to the vascular endothelium is enhanced during tissue ischemia and/or inflammation, conditions that are associated with tissue acidosis. This study examined the effects of hypercarbic acidosis (10 or 20% CO2) and of hypocarbic alkalosis (0% CO2) on human neutrophil CD18 and human aortic endothelial cell intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin expression quantified by flow cytometry. Acidosis with 20% CO2 for 4 h decreased ICAM-1 to 60.6 +/- 9.7% of control. In contrast, alkalosis with 0% CO2 for 4 h enhanced ICAM-1 expression to 143.8 +/- 10.1% of control. There was no pH dependence of VCAM-1 or E-selectin expression. Tumor necrosis factor-alpha (TNF-alpha; 10 ng/ml) increased endothelial ICAM-1, E-selectin, and VCAM-1; under these conditions, acidosis with 20% CO2 blunted both ICAM-1 and E-selectin surface expression compared with 5% CO2-, TNF-alpha-treated cells. Hypercarbic acidosis with 20% CO2 increased neutrophil CD18 expression and enhanced neutrophil adhesion. This latter effect was inhibited by neutrophil pretreatment with an anti-CD18 monoclonal antibody. In contrast, when only endothelial cells were preincubated with the hypercarbic buffer, neutrophil adhesion diminished to 55.6 +/- 7.8% of control. The results suggest that acidosis generated during tissue ischemia/inflammation may induce CD18-mediated neutrophil adhesion despite a decrease in ICAM-1 expression.
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Payan, P., H. De Pontual, A. Edeyer, G. Borelli, G. Boeuf, and N. Mayer-Gostan. "Effects of stress on plasma homeostasis, endolymph chemistry, and check formation during otolith growth in rainbow trout (Oncorhynchus mykiss)." Canadian Journal of Fisheries and Aquatic Sciences 61, no. 7 (July 1, 2004): 1247–55. http://dx.doi.org/10.1139/f04-059.
Full textAbstract:
This is the first study in which the effects of an external stress were analysed at different levels: plasma ho meostasis, endolymph chemistry, and otolith growth. Stress was applied to rainbow trout (Oncorhynchus mykiss) by exposure to Cl2 gas. In the plasma of Cl2-stressed trout, Na+ and Cl decreased (70 mmol·L1) and K+ increased (2.0 mmol·L1), whereas total Ca was unchanged. A slight hypercapny (+2.4 mmHg (1 mmHg = 133.322 Pa)) was observed related to a significant rise (40%) in total CO2 without pH variation. In the endolymph, Na+ and Cl also decreased, whereas other parameters (K+, PO43, Mg, and, peculiarly, total Ca) remained stable. The important effect provoked by Cl2 stress in endolymph was an increase of proteins (factor of 2.6) and total CO2 (factor of 3.1) concentrations at the proximal side of the endolymph. The stress induced a decrease in otolith growth rate and produced a discontinuity (check) in the microstructure pattern of the otolith characterized by a large D zone. The variations in the endolymph composition are discussed and we propose that they result not only from changes in plasma concentrations, but also from changes (organic and crystallization) in otolith deposition.
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Wellner-Kienitz, M. C., H. Shams, and P. Scheid. "Contribution of Ca2+-Activated K+ Channels to Central Chemosensitivity in Cultivated Neurons of Fetal Rat Medulla." Journal of Neurophysiology 79, no. 6 (June 1, 1998): 2885–94. http://dx.doi.org/10.1152/jn.1998.79.6.2885.
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Wellner-Kienitz, M.-C., H. Shams, and P. Scheid. Contribution of Ca2+-activated K+ channels to central chemosensitivity in cultivated neurons of fetal rat medulla. J. Neurophysiol. 79: 2885–2894, 1998. Neurons in fetal rat medullary slices that exhibited spontaneous electrical activity after blockade of synaptic transmission were investigated for their response to decreases in extracellular pH. Increases in [H+] (induced either by fixed acid or increases in PCO2) induced a significant increase in the frequency of action potentials, associated with a membrane depolarization, and/or increases in the slope of the interspike depolarization. In addition, CO2/H+ prolonged the repolarizing phase of action potentials and reduced the afterhyperpolarization, suggesting that K+ channels were the primary site of CO2/H+ action. The type of K+ channel that was modulated by CO2/H+ was identified by application of agents that inhibited Ca2+-activated K+ channels either directly (tetraethylammonium chloride, TEA) or indirectly (Cd2+ ions) by inhibiting Ca2+ influx. CO2/H+ effects on neuronal activity were abolished after application of these blockers. The contribution of Ca2+-activated K+ channels to H+ sensitivity of these neurons was confirmed further in voltage-clamp experiments in which outward rectifying I-V curves were recorded that revealed a zero current potential of −70 mV. CO2/H+ induced a prominent reduction in outward currents and shifted the zero current potential to more positive membrane potentials (mean −63 mV). The CO2/H+-sensitive current reversed at −72 mV and was blocked by external application of TEA. It is concluded that CO2/H+ exerts its stimulatory effects on fetal medullary neurons by inhibition of Ca2+-activated K+ channels, either directly or indirectly, by blocking voltage-dependent Ca2+ channels, which in turn results in a reduction of K+ efflux and in cell depolarization.
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Komukai, Kimiaki, Tetsuya Ishikawa, and Satoshi Kurihara. "Effects of acidosis on Ca2+sensitivity of contractile elements in intact ferret myocardium." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 1 (January 1, 1998): H147—H154. http://dx.doi.org/10.1152/ajpheart.1998.274.1.h147.
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We investigated the effects of acidosis on the intracellular Ca2+ concentration ([Ca2+]i) and contractile properties of intact mammalian cardiac muscle during tetanic and twitch contractions. Aequorin was injected into ferret papillary muscles, and the [Ca2+]iand tension were simultaneously measured. Acidosis was attained by increasing the CO2 concentration in the bicarbonate (20 mM)-buffered Tyrode solution from 5% (pH 7.35, control) to 15% (pH 6.89, acidosis). Tetanic contraction was produced by repetitive stimulation of the preparation following treatment with 5 μM ryanodine. The relationship between [Ca2+]iand tension was measured 6 s after the onset of the stimulation and was fitted using the Hill equation. Acidosis decreased the maximal tension to 81 ± 2% of the control and shifted the [Ca2+]i-tension relationship to the right by 0.18 ± 0.01 pCa units. During twitch contraction, a quick shortening of muscle length from the length at which developed tension became maximal ( L max) to 92% L maxproduced a transient change in the [Ca2+]i(extra Ca2+). The magnitude of the extra Ca2+ was dependent on the [Ca2+]iimmediately before the length change, suggesting that the extra Ca2+ is related to the amount of troponin-Ca complex. Acidosis decreased the normalized extra Ca2+ to [Ca2+]iimmediately before the length change, which indicates that the amount of Ca2+ bound to troponin C is less when [Ca2+]iis the same as in the control. The decrease in the Ca2+ binding to troponin C explains the decrease in tetanic and twitch contraction, and mechanical stress applied to the preparation induced less [Ca2+]ichange in acidosis.
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Lyall, Vijay, Rammy I. Alam, Duy Q. Phan, Glenn L. Ereso, Tam-Hao T. Phan, Shahbaz A. Malik, Marshall H. Montrose, et al. "Decrease in rat taste receptor cell intracellular pH is the proximate stimulus in sour taste transduction." American Journal of Physiology-Cell Physiology 281, no. 3 (September 1, 2001): C1005—C1013. http://dx.doi.org/10.1152/ajpcell.2001.281.3.c1005.
Full textAbstract:
Taste receptor cells (TRCs) respond to acid stimulation, initiating perception of sour taste. Paradoxically, the pH of weak acidic stimuli correlates poorly with the perception of their sourness. A fundamental issue surrounding sour taste reception is the identity of the sour stimulus. We tested the hypothesis that acids induce sour taste perception by penetrating plasma membranes as H+ ions or as undissociated molecules and decreasing the intracellular pH (pHi) of TRCs. Our data suggest that taste nerve responses to weak acids (acetic acid and CO2) are independent of stimulus pH but strongly correlate with the intracellular acidification of polarized TRCs. Taste nerve responses to CO2 were voltage sensitive and were blocked with MK-417, a specific blocker of carbonic anhydrase. Strong acids (HCl) decrease pHi in a subset of TRCs that contain a pathway for H+ entry. Both the apical membrane and the paracellular shunt pathway restrict H+ entry such that a large decrease in apical pH is translated into a relatively small change in TRC pHi within the physiological range. We conclude that a decrease in TRC pHi is the proximate stimulus in rat sour taste transduction.
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Holcroft, Deirdre M., and Adel A. Kader. "Carbon Dioxide–induced Changes in Color and Anthocyanin Synthesis of Stored Strawberry Fruit." HortScience 34, no. 7 (December 1999): 1244–48. http://dx.doi.org/10.21273/hortsci.34.7.1244.
Full textAbstract:
Anthocyanin concentrations increased in both external and internal tissues of `Selva' strawberries (Fragaria ×ananassa Duch.) stored in air at 5 °C for 10 days, but the increase was lower in fruit stored in air enriched with 10 or 20 kPa CO2. Flesh red color was less intense in CO2 storage than in air storage. Activities of phenylalanine ammonia lyase (PAL) and UDP glucose: flavonoid glucosyltransferase (GT) decreased during storage, with decreases being greater in both external and internal tissues of strawberry fruit stored in air + 20 kPa CO2 than in those kept in air. Activities of both PAL and GT in external tissues of strawberries stored in air + 10 kPa CO2 were similar to those in fruit stored in air, while enzyme activities in internal tissues more closely resembled those from fruit stored in air + 20 kPa CO2. Phenolic compounds increased during storage but were not affected by the storage atmosphere. The pH increased and titratable acidity decreased during storage; these effects were enhanced in internal tissues by the CO2 treatments, and may in turn have influenced anthocyanin expression.
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Stenkamp, Kerstin, J. Matias Palva, Marylka Uusisaari, Sebastian Schuchmann, Dietmar Schmitz, Uwe Heinemann, and Kai Kaila. "Enhanced Temporal Stability of Cholinergic Hippocampal Gamma Oscillations Following Respiratory Alkalosis In Vitro." Journal of Neurophysiology 85, no. 5 (May 1, 2001): 2063–69. http://dx.doi.org/10.1152/jn.2001.85.5.2063.
Full textAbstract:
The decrease in brain CO2 partial pressure (pCO2) that takes place both during voluntary and during pathological hyperventilation is known to induce gross alterations in cortical functions that lead to subjective sensations and altered states of consciousness. The mechanisms that mediate the effects of the decrease in pCO2 at the neuronal network level are largely unexplored. In the present work, the modulation of gamma oscillations by hypocapnia was studied in rat hippocampal slices. Field potential oscillations were induced by the cholinergic agonist carbachol under an N-methyl-D-aspartate (NMDA)-receptor blockade and were recorded in the dendritic layer of the CA3 region with parallel measurements of changes in interstitial and intraneuronal pH (pHo and pHi, respectively). Hypocapnia from 5 to 1% CO2 led to a stable monophasic increase of 0.5 and 0.2 units in pHo and pHi, respectively. The mean oscillation frequency increased slightly but significantly from 32 to 34 Hz and the mean gamma-band amplitude (20 to 80 Hz) decreased by 20%. Hypocapnia induced a dramatic enhancement of the temporal stability of the oscillations, as was indicated by a two-fold increase in the exponential decay time constant fitted to the autocorrelogram. A rise in pHi evoked by the weak base trimethylamine (TriMA) was associated with a slight increase in oscillation frequency (37 to 39 Hz) and a decrease in amplitude (30%). Temporal stability, on the other hand, was decreased by TriMA, which suggests that its enhancement in 1% CO2 was related to the rise in pHo. In 1% CO2, the decay-time constant of the evoked monosynaptic pyramidal inhibitory postsynaptic current (IPSC) was unaltered but its amplitude was enhanced. This increase in IPSC amplitude seems to significantly contribute to the enhancement of temporal stability because the enhancement was almost fully reversed by a low concentration of bicuculline. These results suggest that changes in brain pCO2 can have a strong influence on the temporal modulation of gamma rhythms.
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Cicha, Iwona, Yoji Suzuki, Norihiko Tateishi, and Nobuji Maeda. "Changes of RBC aggregation in oxygenation-deoxygenation: pH dependency and cell morphology." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 6 (June 1, 2003): H2335—H2342. http://dx.doi.org/10.1152/ajpheart.01030.2002.
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The effects of the oxygenation-deoxygenation process on red blood cell (RBC) aggregation were examined in relation to morphological changes in RBCs and the contribution of CO2. A low-shear rheoscope was used to measure the rate of rouleaux (one-dimensional aggregate) formation in diluted autologous plasma exposed to gas mixtures with different Po 2 and Pco 2. RBC indexes and RBC suspension pH were measured for the oxygenated or the deoxygenated condition, and the cell shape was observed with a scanning electron microscope. In the oxygenation-deoxygenation process, the rate of rouleaux formation increased with rising pH of the RBC suspension, which was lowered in the presence of CO2. The rate increased with increasing mean corpuscular hemoglobin concentration (thus the cells shrank), which increased with rising pH and decreased in the presence of CO2. With rising pH, cell diameter increased and cell thickness decreased (thus the cell flattened). In addition, slight echinocytosis was induced in the presence of CO2, and the aggregation was reduced by the morphological change. In conclusion, RBC aggregation in the oxygenation-deoxygenation process is mainly influenced by the pH-dependent change in the surface area-to-volume ratio of the cells, and the aggregation is modified by CO2-induced acidification and the accompanying changes in mean corpuscular hemoglobin concentration and cell shape.
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Lückermann, Mark, Stefan Trapp, and Klaus Ballanyi. "GABA- and Glycine-Mediated Fall of Intracellular pH in Rat Medullary Neurons In Situ." Journal of Neurophysiology 77, no. 4 (April 1, 1997): 1844–52. http://dx.doi.org/10.1152/jn.1997.77.4.1844.
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Lückermann, Mark, Stefan Trapp, and Klaus Ballanyi. GABA- and glycine-mediated fall of intracellular pH in rat medullary neurons in situ. J. Neurophysiol. 77: 1844–1852, 1997. In the region of the ventral respiratory group in brain stem slices from neonatal rats, intracellular pH (pHi) and membrane currents ( I m) or potentials were measured in neurons dialyzed with the pH-sensitive dye 2′,7′-bis-carboxyethyl-5(6)-carboxyfluorescein. Currents and increases in membrane conductance ( g m) during bath application of 0.1 or 1 mM γ-aminobutyric acid (GABA) were accompanied by a delayed mean fall of pHi by 0.17 and 0.25 pH units, respectively, from a pHi baseline of 7.33. These effects were reversibly suppressed by 50–100 μM bicuculline. Similar effects on I m, g m, and pHi were revealed on administration of 0.1 or 1 mM glycine. These responses were abolished by 10–100 μM strychnine. Dialysis of the cells with 15–30 μM carbonic anhydrase led to an acceleration of the kinetics and a potentiation of the GABA-induced pHi decrease. GABA- and glycine-evoked pHi decreases were very similar during recordings with either high- or low-Cl− patch electrodes, although the reversal potential of the accompanying currents differed by ∼60 mV. The GABA-induced pHi decrease, but not the accompanying I m and g m responses, was suppressed in CO2/HCO− 3-free, N-2-hydroxy-ethylpiperazine- N′-2-ethane sulphonic acid pH-buffered solution. Depolarization from −60 to +30 mV resulted in a sustained fall of pHi by maximally 0.5 pH units. In this situation, the GABA-induced fall of pHi turned into an intracellular alkalosis of 0.09–0.15 pH units. The results confirm and extend previous findings obtained in vivo that GABA- or glycine-induced intracellular acidosis of respiratory neurons is due to efflux of HCO− 3 via the receptor-coupled Cl− channel.
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Brody, L. R., M. T. Pollock, S. H. Roy, C. J. De Luca, and B. Celli. "pH-induced effects on median frequency and conduction velocity of the myoelectric signal." Journal of Applied Physiology 71, no. 5 (November 1, 1991): 1878–85. http://dx.doi.org/10.1152/jappl.1991.71.5.1878.
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H+ accumulation at the sarcolemma is believed to play a key role in determining the electrophysiological correlates of fatigue. This paper describes an in vitro method to externally manipulate muscle pH while measuring the resultant effect on surface-detected median frequency (MDF) and conduction velocity (CV) parameters. Hamster muscle diaphragm strips (n = 8) were isolated with the phrenic nerve intact and placed in an oxygenated Krebs bath (26 degrees C). The muscle was clamped to a noncompliant load cell to measure isometric contractile tension. Tetanic contraction was developed via 40-Hz supermaximal stimulation of the phrenic nerve. Differential signals were recorded from three electromyogram (EMG) detection surfaces for computation of CV (via the phase shift in the EMG signals) and MDF. Repeated trials were conducted at bath pHs of 7.4, 7.0, and 6.6. Bath pH was altered by aerating predetermined concentrations of O2 and CO2 into the bath. Decreases in bath pH resulted in decreases in both initial MDF and initial CV. The differences in initial MDF and initial CV were significant (P less than 0.001) for each of the bath pH conditions. In general, the change in bath pH resulted in an equal percent change in initial MDF and initial CV. This suggests that the change in bath pH caused a decrease in CV without significantly altering the fundamental shape of the M wave. In contrast, the EMG was altered differently during stimulated contractions. During stimulation, the rate of decay of CV was 65% of the rate of decay of MDF.(ABSTRACT TRUNCATED AT 250 WORDS)
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Yang, Tao-Yu, Li-Ya Cai, Yi-Ping Qi, Lin-Tong Yang, Ning-Wei Lai, and Li-Song Chen. "Increasing Nutrient Solution pH Alleviated Aluminum-Induced Inhibition of Growth and Impairment of Photosynthetic Electron Transport Chain in Citrus sinensis Seedlings." BioMed Research International 2019 (August 27, 2019): 1–17. http://dx.doi.org/10.1155/2019/9058715.
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Although the physiological and molecular responses of Citrus to Al-toxicity or low pH have been examined in some details, little information is available on Citrus responses to pH and aluminum (Al) interactions. Citrus sinensis seedlings were irrigated for 18 weeks with nutrient solution at a concentration of 0 or 1 mM AlCl3•6H2O and a pH of 2.5, 3.0, 3.5, or 4.0. Thereafter, biomass, root, stem, and leaf concentrations of Al and nutrients, leaf gas exchange, chlorophyll a fluorescence (OJIP) transients, and related parameters were investigated to understand the physiological mechanisms underlying the elevated pH-induced alleviation of Citrus toxicity. Increasing the nutrient solution pH from 2.5 to 4.0 alleviated the Al-toxic effects on biomass, photosynthesis, OJIP transients and related parameters, and element concentrations, uptake, and distributions. In addition, low pH effects on the above physiological parameters were intensified by Al-toxicity. Evidently, a synergism existed between low pH and Al-toxicity. Increasing pH decreased Al uptake per root dry weight and its concentration in roots, stems, and leaves and increased nitrogen, phosphorus, calcium, magnesium, sulfur, and boron uptake per plant and their concentrations in roots, stems, and leaves. This might be responsible for the elevated pH-induced alleviation of growth inhibition and the impairment of the whole photosynthetic electron transport chain, thus preventing the decrease of CO2 assimilation.
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Katsura, Ken-Ichiro, Tibor Kristián, Maj-Lis Smith, and Bo K. Siesjö. "Acidosis Induced by Hypercapnia Exaggerates Ischemic Brain Damage." Journal of Cerebral Blood Flow & Metabolism 14, no. 2 (March 1994): 243–50. http://dx.doi.org/10.1038/jcbfm.1994.31.
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Although preischemic hyperglycemia is known to aggravate damage due to transient ischemia, it is a matter of controversy whether or not this is a result of the exaggerated acidosis. It has recently been reported that although tissue acidosis of a comparable severity could be induced in normoglycemic dogs by an excessive rise in arterial CO2 tension, short-term functional recovery was improved, rather than compromised. In the present experiments we induced excessive hypercapnia (Paco2, ∼300 mm Hg) in normoglycemic rats before inducing forebrain ischemia of 10-min duration. This reduced the brain extracellular pH to values normally encountered in hyperglycemic rats subjected to ischemia. The events induced by hypercapnia clearly enhanced ischemic brain damage, as assessed histologically after 7 days of recovery. We hypothesize that the decisive event was an exaggerated decrease in extra- and intracellular pH and that the results thus demonstrate an adverse effect of acidosis. However, since postischemic seizures did not occur in the hypercapnic ischemic rats, the results also demonstrate that changes in intra-extracellular pH and bicarbonate concentrations modulated ischemic damage in an unexpected way.
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Wu, Mei-Lin, Jeng-Haur Chen, Wei-Hao Chen, Yu-Jen Chen, and Kuan-Chou Chu. "Novel role of the Ca2+-ATPase in NMDA-induced intracellular acidification." American Journal of Physiology-Cell Physiology 277, no. 4 (October 1, 1999): C717—C727. http://dx.doi.org/10.1152/ajpcell.1999.277.4.c717.
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The mechanism involved in N-methyl-d-glucamine (NMDA)-induced Ca2+-dependent intracellular acidosis is not clear. In this study, we investigated in detail several possible mechanisms using cultured rat cerebellar granule cells and microfluorometry [fura 2-AM or 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein-AM]. When 100 μM NMDA or 40 mM KCl was added, a marked increase in the intracellular Ca2+ concentration ([Ca2+]i) and a decrease in the intracellular pH were seen. Acidosis was completely prevented by the use of Ca2+-free medium or 1,2-bis(2-aminophenoxy)ethane- N, N, N′, N′-tetraacetic acid-AM, suggesting that it resulted from an influx of extracellular Ca2+. The following four mechanisms that could conceivably have been involved were excluded: 1) Ca2+ displacement of intracellular H+ from common binding sites; 2) activation of an acid loader or inhibition of acid extruders; 3) overproduction of CO2 or lactate; and 4) collapse of the mitochondrial membrane potential due to Ca2+uptake, resulting in inhibition of cytosolic H+ uptake. However, NMDA/KCl-induced acidosis was largely prevented by glycolytic inhibitors (iodoacetate or deoxyglucose in glucose-free medium) or by inhibitors of the Ca2+-ATPase (i.e., Ca2+/H+exchanger), including La3+, orthovanadate, eosin B, or an extracellular pH of 8.5. Our results therefore suggest that Ca2+-ATPase is involved in NMDA-induced intracellular acidosis in granule cells. We also provide new evidence that NMDA-evoked intracellular acidosis probably serves as a negative feedback signal, probably with the acidification itself inhibiting the NMDA-induced [Ca2+]iincrease.
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Ninokawa, Aaron T., and Justin Ries. "Responses of Freshwater Calcifiers to Carbon-Dioxide-Induced Acidification." Journal of Marine Science and Engineering 10, no. 8 (August 4, 2022): 1068. http://dx.doi.org/10.3390/jmse10081068.
Full textAbstract:
Increased anthropogenic carbon dioxide (CO2) in the atmosphere can enter surface waters and depress pH. In marine systems, this phenomenon, termed ocean acidification (OA), can modify a variety of physiological, ecological, and chemical processes. Shell-forming organisms are particularly sensitive to this chemical shift, though responses vary amongst taxa. Although analogous chemical changes occur in freshwater systems via absorption of CO2 into lakes, rivers, and streams, effects on freshwater calcifiers have received far less attention, despite the ecological importance of these organisms to freshwater systems. We exposed four common and widespread species of freshwater calcifiers to a range of pCO2 conditions to determine how CO2-induced reductions in freshwater pH impact calcium carbonate shell formation. We incubated the signal crayfish, Pacifastacus leniusculus, the Asian clam, Corbicula fluminea, the montane pea clam, Pisidium sp., and the eastern pearlshell mussel, Margaritifera margaritifera, under low pCO2 conditions (pCO2 = 616 ± 151 µatm; pH = 7.91 ± 0.11), under moderately elevated pCO2 conditions (pCO2 = 1026 ± 239 uatm; pH = 7.67 ± 0.10), and under extremely elevated pCO2 conditions (pCO2 = 2380 ± 693 uatm; pH = 7.32 ± 0.12). Three of these species exhibited a negative linear response to increasing pCO2 (decreasing pH), while the fourth, the pea clam, exhibited a parabolic response. Additional experiments revealed that feeding rates of the crayfish decreased under the highest pCO2 treatment, potentially contributing to or driving the negative calcification response of the crayfish to elevated pCO2 by depriving them of energy needed for biocalcification. These results highlight the potential for freshwater taxa to be deleteriously impacted by increased atmospheric pCO2, the variable nature of these responses, and the need for further study of this process in freshwater systems.
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Orr, L. A., and E. M. Lieberman. "Studies of the cardiac-like action potential in crayfish giant axons induced by platinized tungsten metal electrodes." Journal of Experimental Biology 128, no. 1 (March 1, 1987): 1–17. http://dx.doi.org/10.1242/jeb.128.1.1.
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A lightly platinized tungsten (Pt-W) wire electrode, axially inserted into a crayfish giant axon, causes the development of cardiac-like action potentials with durations of up to 4 s. The plateau in membrane potential typically occurs within 10 min of the start of action potential elongation. The effect occurs without passing current through the Pt-W electrode and is temporally related to a dramatic decrease in intracellular pH (pHi). Such an effect cannot be induced by a decrease in pHi produced by equilibrating the axon with HCO3(−)-CO2 solution (pH6), and NH4Cl rebound or direct intracellular injection of PO4(3-) buffer (pH 4 X 5). Action potential elongation is accompanied by a block of delayed rectification and the possibility that inward rectification also develops cannot be ruled out. Plateau generation requires Na+ and Ca2+ inward currents as demonstrated by abolition of the plateau by [Na+]o or [Ca2+]o depletion or treatment with tetrodotoxin (TTX) or verapamil. The block of outward rectification by Pt-W requires external Na+ or Ca2+. Action potential elongation produced by 3,4-diaminopyridine is not sensitive to verapamil and the waveform is different from that produced by Pt-W. The data support the possibility that different classes of excitable membranes have similar channel populations and that the functional differences between them reside in the inhibitory or masking influences that are present in the microenvironments of the various membrane channels.
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Mattiazzi, A., N. G. Perez, M. G. Vila-Petroff, B. Alvarez, M. C. Camilion de Hurtado, and H. E. Cingolani. "Dissociation between positive inotropic and alkalinizing effects of angiotensin II in feline myocardium." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 3 (March 1, 1997): H1131—H1136. http://dx.doi.org/10.1152/ajpheart.1997.272.3.h1131.
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The present study examines the intracellular pH (pHi) dependence of angiotensin (ANG) II-induced positive inotropic effect in cat papillary muscles contracting isometrically (0.2 Hz, 30 degrees C). Muscles were loaded with the fluorescent dye 2'-7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein acetoxymethyl ester for simultaneous measurement of pHi and contractility. In N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) buffer (n = 4), there was a temporal dissociation between the positive inotropic and the alkalinizing effects of ANG II (0.5 microM). The positive inotropic effect of ANG II peaked at 9.7 +/- 0.8 min (240 +/- 57% above control) without significant changes in pHi. The increase in pHi became significant (0.05 +/- 0.01 pH units) only after 16 min of exposure to the drug, when the positive inotropic effect of ANG II was already fading. In HCO3- buffer (n = 7), the ANG II-induced positive inotropic effect occurred without significant pHi changes. In the presence of 5 microM ethyl isopropyl amiloride (EIPA, to specifically inhibit the Na+/H+ exchanger), the alkalinizing effect of ANG II was changed to a significant decrease in pHi, despite which ANG II still increased contractility by 87 +/- 16% (n = 6). The results indicate that in HEPES buffer only a fraction of the ANG II-induced positive inotropic effect can be attributed to a pHi change, whereas in a physiological CO2-HCO3- medium the positive inotropic effect of ANG II is independent of pHi changes. Furthermore, an ANG II-induced increase in myocardial contractility was observed even when ANG II administration elicited a decrease in pHi, as occurred after Na+/H+ exchanger blockade. The results show that in feline myocardium, the increase in contractility evoked by ANG II in a physiological CO2-HCO3- medium is not due to an increase in Ca2+ myofilament sensitivity secondary to an increase in myocardial pHi.
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Wu, Y., K. Gao, and U. Riebesell. "CO<sub>2</sub>-induced seawater acidification affects physiological performance of the marine diatom <I>Phaeodactylum tricornutum</I>." Biogeosciences Discussions 7, no. 3 (May 25, 2010): 3855–78. http://dx.doi.org/10.5194/bgd-7-3855-2010.
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Abstract. CO2/pH perturbation experiments were carried out under two different pCO2 levels (39.3 and 101.3 Pa) to evaluate effects of CO2-induced ocean acidification on the marine diatom Phaeodactylum tricornutum. After acclimation (>20 generations) to ambient and elevated CO2 conditions (with corresponding pH values of 8.15 and 7.80, respectively), growth and photosynthetic carbon fixation rates of high CO2 grown cells were enhanced by 5% and 12%, respectively, and dark respiration stimulated by 34% compared to cells grown at ambient CO2. The K1/2 (dissolved inorganic carbon, DIC) for carbon fixation increased by 20% under the low pH and high CO2 condition, reflecting a decreased photosynthetic affinity for HCO3− or/and CO2 and down-regulated carbon concentrating mechanism (CCM). In the high CO2 grown cells, the electron transport rate from photosystem II (PSII) was photoinhibited to a greater extent at high levels of photosynthetically active radiation, while non-photochemical quenching was reduced compared to low CO2 grown cells. This was probably due to the down-regulation of CCM, which serves as a sink for excessive energy. Increasing seawater pCO2 and decreasing pH associated with atmospheric CO2 rise may enhance diatom growth, down-regulate their CCM, and enhanced their photo-inhibition and dark respiration. The balance between these positive and negative effects on diatom productivity will be a key factor in determining the net effect of rising atmospheric CO2 on ocean primary production.
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Alharbi, Ahad Abdulkarim D., Naoyuki Ebine, Satoshi Nakae, Tatsuya Hojo, and Yoshiyuki Fukuoka. "Application of Molecular Hydrogen as an Antioxidant in Responses to Ventilatory and Ergogenic Adjustments during Incremental Exercise in Humans." Nutrients 13, no. 2 (January 30, 2021): 459. http://dx.doi.org/10.3390/nu13020459.
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We investigated effects of molecular hydrogen (H2) supplementation on acid-base status, pulmonary gas exchange responses, and local muscle oxygenation during incremental exercise. Eighteen healthy, trained subjects in a randomized, double-blind, crossover design received H2-rich calcium powder (HCP) (1500 mg/day, containing 2.544 µg/day of H2) or H2-depleted placebo (1500 mg/day) for three consecutive days. They performed cycling incremental exercise starting at 20-watt work rate, increasing by 20 watts/2 min until exhaustion. Breath-by-breath pulmonary ventilation (V˙E) and CO2 output (V˙CO2) were measured and muscle deoxygenation (deoxy[Hb + Mb]) was determined via time-resolved near-infrared spectroscopy in the vastus lateralis (VL) and rectus femoris (RF). Blood gases’ pH, lactate, and bicarbonate (HCO3−) concentrations were measured at rest and 120-, 200-, and 240-watt work rates. At rest, the HCP group had significantly lower V˙E, V˙CO2, and higher HCO3−, partial pressures of CO2 (PCO2) versus placebo. During exercise, a significant pH decrease and greater HCO3− continued until 240-watt workload in HCP. The V˙E was significantly lower in HCP versus placebo, but HCP did not affect the gas exchange status of V˙CO2 or oxygen uptake (V˙O2). HCP increased absolute values of deoxy[Hb + Mb] at the RF but not VL. Thus, HCP-induced hypoventilation would lead to lower pH and secondarily impaired balance between O2 delivery and utilization in the local RF during exercise, suggesting that HCP supplementation, which increases the at-rest antioxidant potential, affects the lower ventilation and pH status during incremental exercise. HPC induced a significantly lower O2 delivery/utilization ratio in the RF but not the VL, which may be because these regions possess inherently different vascular/metabolic control properties, perhaps related to fiber-type composition.
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Wu, Y., K. Gao, and U. Riebesell. "CO<sub>2</sub>-induced seawater acidification affects physiological performance of the marine diatom <i>Phaeodactylum tricornutum</i>." Biogeosciences 7, no. 9 (September 24, 2010): 2915–23. http://dx.doi.org/10.5194/bg-7-2915-2010.
Full textAbstract:
Abstract. CO2/pH perturbation experiments were carried out under two different pCO2 levels (39.3 and 101.3 Pa) to evaluate effects of CO2-induced ocean acidification on the marine diatom Phaeodactylum tricornutum. After acclimation (>20 generations) to ambient and elevated CO2 conditions (with corresponding pH values of 8.15 and 7.80, respectively), growth and photosynthetic carbon fixation rates of high CO2 grown cells were enhanced by 5% and 12%, respectively, and dark respiration stimulated by 34% compared to cells grown at ambient CO2. The half saturation constant (Km) for carbon fixation (dissolved inorganic carbon, DIC) increased by 20% under the low pH and high CO2 condition, reflecting a decreased affinity for HCO3– or/and CO2 and down-regulated carbon concentrating mechanism (CCM). In the high CO2 grown cells, the electron transport rate from photosystem II (PSII) was photoinhibited to a greater extent at high levels of photosynthetically active radiation, while non-photochemical quenching was reduced compared to low CO2 grown cells. This was probably due to the down-regulation of CCM, which serves as a sink for excessive energy. The balance between these positive and negative effects on diatom productivity will be a key factor in determining the net effect of rising atmospheric CO2 on ocean primary production.
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Li, Aihua, and Eugene E. Nattie. "Focal central chemoreceptor sensitivity in the RTN studied with a CO2 diffusion pipette in vivo." Journal of Applied Physiology 83, no. 2 (August 1, 1997): 420–28. http://dx.doi.org/10.1152/jappl.1997.83.2.420.
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Li, Aihua, and Eugene E. Nattie. Focal central chemoreceptor sensitivity in the RTN studied with a CO2 diffusion pipette in vivo. J. Appl. Physiol. 83(2): 420–428, 1997.—We describe and use a CO2diffusion pipette to produce a quickly reversible focal acidosis in the retrotrapezoid nucleus region of the rat brain stem. No tissue injection is made. Instead, artificial cerebrospinal fluid (aCSF) equilibrated with CO2 circulates within the micropipette, providing a source for continued CO2 diffusion into the tissue from the pipette tip. Tissue pH electrodes show the acidosis is limited to 500 μm from the tip. In controls (aCSF equilibrated with air), 1-min pipette perfusions increased tissue pH slightly and decreased phrenic nerve amplitude. In moderate- and high-CO2 groups (aCSF equilibrated with 50 or 100% CO2), 1-min perfusions significantly decreased tissue pH and increased phrenic nerve amplitude in a dose-dependent manner. The responses developed and reversed within minutes. Compared with our prior use of medullary acetazolamide injections to produce a focal acidosis, in this approach the acidosis 1) arises and reverses quickly and 2) its intensity can be varied. This allows study of sensitivity and mechanism. We conclude from this initial experiment that retrotrapezoid nucleus region chemoreceptors operate within the normal physiological range of CO2-induced tissue pH changes.
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Salameh, Ahlam Ibrahim, Vernon A. Ruffin, and Walter F. Boron. "Effects of metabolic acidosis on intracellular pH responses in multiple cell types." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 307, no. 12 (December 15, 2014): R1413—R1427. http://dx.doi.org/10.1152/ajpregu.00154.2014.
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Metabolic acidosis (MAc), a decrease in extracellular pH (pHo) caused by a decrease in [HCO3−]o at a fixed [CO2]o, is a common clinical condition and causes intracellular pH (pHi) to fall. Although previous work has suggested that MAc-induced decreases in pHi (ΔpHi) differ among cell types, what is not clear is the extent to which these differences are the result of the wide variety of methodologies employed by various investigators. In the present study, we evaluated the effects of two sequential MAc challenges (MAc1 and MAc2) on pHi in 10 cell types/lines: primary-cultured hippocampal (HCN) neurons and astrocytes (HCA), primary-cultured medullary raphé (MRN) neurons, and astrocytes (MRA), CT26 colon cancer, the C2C12 skeletal muscles, primary-cultured bone marrow-derived macrophages (BMDM) and dendritic cells (BMDC), Ink4a/ARF-null melanocytes, and XB-2 keratinocytes. We monitor pHi using ratiometric fluorescence imaging of 2′,7′-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein while imposing MAc: lowering (pHo) from 7.4 to 7.2 by decreasing [HCO3−]o from 22 to 14 mM at 5% CO2 for 7 min. After MAc1, we return cells to the control solution for 10 min and impose MAc2. Using our definition of MAc resistance [(ΔpHi/ΔpHo) ≤ 40%], during MAc1, ∼70% of CT26 and ∼50% of C2C12 are MAc-resistant, whereas the other cell types are predominantly MAc-sensitive. During MAc2, some cells adapt [(ΔpHi/ΔpHo)2 < (ΔpHi/ΔpHo)1], particularly HCA, C2C12, and BMDC. Most maintain consistent responses [(ΔpHi/ΔpHo)2 ≅ (ΔpHi/ΔpHo)1], and a few decompensate [(ΔpHi/ΔpHo)2>(ΔpHi/ΔpHo)1], particularly HCN, C2C12, and XB-2. Thus, responses to twin MAc challenges depend both on the individual cell and cell type.
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Menna, G., C. K. Tong, and M. Chesler. "Extracellular pH Changes and Accompanying Cation Shifts During Ouabain-Induced Spreading Depression." Journal of Neurophysiology 83, no. 3 (March 1, 2000): 1338–45. http://dx.doi.org/10.1152/jn.2000.83.3.1338.
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Interstitial ionic shifts that accompany ouabain-induced spreading depression (SD) were studied in rat hippocampal and cortical slices in the presence and absence of extracellular Ca2+. A double-barreled ion-selective microelectrode specific for H+, K+, Na+, or Ca2+ was placed in the CA1 stratum radiatum or midcortical layer. Superfusion of 100 μM ouabain caused a rapid, negative, interstitial voltage shift (2–10 mV) after 3–5 min. The negativity was accompanied by a rapid alkaline transient followed by prolonged acidosis. In media containing 3 mM Ca2+, the alkalosis induced by ouabain averaged 0.07 ± 0.01 unit pH. In media with no added Ca2+ and 2 mM EGTA, the alkaline shift was not significantly different (0.09 ± 0.02 unit pH). The alkaline transient was unaffected by inhibiting Na+-H+ exchange with ethylisopropylamiloride (EIPA) or by blocking endoplasmic reticulum Ca2+ uptake with thapsigargin or cyclopiazonic acid. Alkaline transients were also observed in Ca2+-free media when SD was induced by microinjecting high K+. The late acidification accompanying ouabain-induced SD was significantly reduced in Ca2+-free media and in solutions containing EIPA. The ouabain-induced SD was associated with a rapid but relatively modest increase in [K+]o. In the presence of 3 mM external Ca2+, the mean peak elevation of [K+]o was 12 ± 0.62 mM. In Ca2+-free media, the elevation of [K+]o had a more gradual onset and reached a significantly larger peak value, which averaged 22 ± 1.1 mM. The decrease in [Na+]o that accompanied ouabain-induced SD was somewhat greater. The [Na+]o decreased by averages of 40 ± 7 and 33 ± 3 mM in Ca2+ and Ca2+-free media, respectively. In media containing 1.2 mM Ca2+, ouabain-induced SD was associated with a substantial decrease in [Ca2+]o that averaged 0.73 ± 0.07 mM. These data demonstrate that in comparison with conventional SD, ouabain-induced SD exhibits ion shifts that are qualitatively similar but quantitatively diminished. The presence of external Ca2+ can modulate the phenomenon but is irrelevant to the generation of the SD and its accompanying alkaline pH transient. Significance of these results is discussed in reference to the propagation of SD and the generation of interstitial pH changes.
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Komukai, Kimiaki, Fabien Brette, Caroline Pascarel, and Clive H. Orchard. "Electrophysiological response of rat ventricular myocytes to acidosis." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 1 (July 1, 2002): H412—H422. http://dx.doi.org/10.1152/ajpheart.01042.2001.
Full textAbstract:
The effects of acidosis on the action potential, resting potential, L-type Ca2+( I Ca), inward rectifier potassium ( I K1), delayed rectifier potassium ( I K), steady-state ( I SS), and inwardly rectifying chloride ( I Cl,ir) currents of rat subepicardial (Epi) and subendocardial (Endo) ventricular myocytes were investigated using the patch-clamp technique. Action potential duration was shorter in Epi than in Endo cells. Acidosis (extracellular pH decreased from 7.4 to 6.5) depolarized the resting membrane potential and prolonged the time for 50% repolarization of the action potential in Epi and Endo cells, although the prolongation was larger in Endo cells. At control pH, I Ca, I K1, and I SS were not significantly different in Epi and Endo cells, but I K was larger in Epi cells. Acidosis did not alter I Ca, I K1, or I K but decreased I SS; this decrease was larger in Endo cells. It is suggested that the acidosis-induced decrease in I SS underlies the prolongation of the action potential. I Cl,ir at control pH was Cd2+ sensitive but 4,4′-disothiocyanato-stilbene-2,2′-disulfonic acid resistant. Acidosis increased I Cl,ir; it is suggested that the acidosis-induced increase in I Cl,ir underlies the depolarization of the resting membrane potential.
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Keller, S. K., T. J. Jentsch, M. Koch, and M. Wiederholt. "Interactions of pH and K+ conductance in cultured bovine retinal pigment epithelial cells." American Journal of Physiology-Cell Physiology 250, no. 1 (January 1, 1986): C124—C137. http://dx.doi.org/10.1152/ajpcell.1986.250.1.c124.
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Passive ion transport properties were studied in confluent monolayers of cultured bovine retinal pigment epithelial cells using intracellular microelectrode technique. The mean stable intracellular (designated by subscript i) potential was -59.1 +/- 0.8 (SE) mV. Extracellular (designated by subscript o) acidification induced a depolarization, whereas alkalinization induced a hyperpolarization. These effects were observed both in bicarbonate-free as well as in HCO3- Ringer (pHo changed by varying [HCO3-]o at constant pCO2). Acidification of pHi (changed by addition and removal of butyrate, CO2 or NH3) also caused a depolarization. Complete removal of HCO3-/CO2 at constant pHo caused a hyperpolarization. K+ transference, checked by applying high K+o, increased with K+o. It decreased with both extra and intracellular acidification and increased with alkalinization. In the presence of Ba2+, voltage reactions to changes in either pHo or pHi were greatly reduced. Depolarization by 40 mM K+ caused a similar reduction. It is suggested that K+ conductance of bovine retinal pigment epithelial cells is reduced by either intra- or extracellular acidification at normal [K+]o. Depolarization by high K+ induces an increase in K+ transference and reduces pH sensitivity.
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Shi, D., Y. Xu, and F. M. M. Morel. "Effects of the pH/<I>p</I>CO<sub>2</sub> control method in the growth medium of phytoplankton." Biogeosciences Discussions 6, no. 1 (February 25, 2009): 2415–39. http://dx.doi.org/10.5194/bgd-6-2415-2009.
Full textAbstract:
Abstract. To study the effects of ocean acidification on the physiology of phytoplankton requires that the key chemical parameters of the growth medium, pCO2, pH and Ω (the saturation state of calcium carbonate) be carefully controlled. This is made difficult by the interdependence of these parameters. Moreover, in growing batch cultures of phytoplankton, the fixation of CO2, the uptake of nutrients and, for coccolithophores, the precipitation of calcite all change the inorganic carbon and acid-base chemistry of the medium. For example, absent pH-buffering or CO2 bubbling, a sizeable decrease in pCO2 occurs at a biomass concentration as low as 50 μM C in non-calcifying cultures. Even in cultures where pCO2 or pH is maintained constant, other chemical parameters change substantially at high cell densities. The quantification of these changes is facilitated by the use of buffer capacities. Experimentally we observe that all methods of adjustment of pCO2/pH can be used, the choice of one or the other depending on the specifics of the experiments. The mechanical effect of bubbling of cultures seems to induce more variable results than other methods of pCO2/pH control. While highly convenient, the addition of pH buffers to the medium induces changes in trace metal availability and cannot be used under trace metal-limiting conditions.
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Boyarsky, G., M. B. Ganz, R. B. Sterzel, and W. F. Boron. "pH regulation in single glomerular mesangial cells. I. Acid extrusion in absence and presence of HCO3-." American Journal of Physiology-Cell Physiology 255, no. 6 (December 1, 1988): C844—C856. http://dx.doi.org/10.1152/ajpcell.1988.255.6.c844.
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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-.
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Litt, Lawrence, Ricardo González-Méndez, John W. Severinghaus, William K. Hamilton, Julia Shuleshko, Joseph Murphy-Boesch, and Thomas L. James. "Cerebral Intracellular Changes during Supercarbia: An in vivo 31P Nuclear Magnetic Resonance Study in Rats." Journal of Cerebral Blood Flow & Metabolism 5, no. 4 (December 1985): 537–44. http://dx.doi.org/10.1038/jcbfm.1985.81.
Full textAbstract:
31P nuclear magnetic resonance (NMR) spectroscopy was used noninvasively to measure in vivo changes in intracellular pH and intracellular phosphate metabolites in the brains of rats during supercarbia (Paco2 ⩾ 400 mm Hg). Five intubated rats were mechanically ventilated with inspired gas mixtures containing 70% CO2 and 30% O2. Supercarbia in the rat was observed to cause a greater reduction in cerebral intracellular pH (pHi) and increase in Pco2 than observed in other experiments with rats after 15 min of global ischemia. Complete neurologic and metabolic recovery was observed in these animals, despite an average decrease in pH; of 0.63 ± 0.02 pH unit during supercarbia episodes that raised Paco2 to 490 ± 80 mm Hg. No change was observed in cerebral intracellular ATP and only a 25% decrease was detected in phosphocreatine. The concentration of free cerebral intracellular ADP, which can be calculated if one assumes that the creatine kinase reaction is in equilibrium, decreased to approximately one-third of its control value. The calculated threefold decrease in the concentration of free ADP and twofold increase in the cytosolic phosphorylation potential suggest that there is increased intracellular oxygenation during supercarbia. Because a more than fourfold increase in intracellular hydrogen ion concentration was tolerated without apparent clinical injury, we conclude that so long as adequate tissue oxygenation and perfusion are maintained, a severe decrease in intracellular pH need not induce or indicate brain injury.
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Inouye, K. "Induction by acid load of the maturation of prestalk cells in Dictyostelium discoideum." Development 104, no. 4 (December 1, 1988): 669–81. http://dx.doi.org/10.1242/dev.104.4.669.
Full textAbstract:
During the process of fruiting body construction in the cellular slime mould Dictyostelium discoideum, prestalk cells become mature stalk cells in a well-controlled manner. To identify the natural inducer of stalk cell maturation, substances known to induce stalk cell differentiation under in vitro conditions, and some other related compounds, were examined for their effects in vivo on migrating slugs, the precursor structures of the fruiting bodies. Among these substances, addition of weak acids such as CO2, and addition followed by removal of weak bases such as NH3, strikingly induced the maturation of prestalk cells in situ in slugs. On the other hand, inhibitors of the plasma membrane proton pump did not efficiently induce the maturation of prestalk cells in intact slugs. Differentiation inducing factor (DIF), an endogenous inducer of prestalk differentiation, seemed to be an even poorer inducer of stalk cell maturation when applied to intact slugs. The activities of these substances in inducing stalk cell maturation showed a good correlation with their effects on the cytoplasmic pH (pHi) of prestalk cells; the larger the pHi drop, the stronger the induction of stalk cell maturation, suggesting a requirement for a pHi decrease for the maturation of prestalk cells. Based on these results, it was proposed that stalk cell differentiation, which is induced by DIF, is blocked halfway during normal development by (an) agent(s) that prevent(s) the decrease in pHi.