scholarly journals The role of intracellular pH in the regulation of cation exchanges in yeast

1972 ◽  
Vol 128 (1) ◽  
pp. 139-146 ◽  
Author(s):  
J. P. Ryan ◽  
H. Ryan
Keyword(s):  
Intracellular Ph ◽  
Extracellular Ph ◽  
K Uptake ◽  
Ph Changes ◽  
Optimum Rate ◽  
Na Efflux

1. When yeast oxidizes propan-2-ol in the presence of KCl no uptake of K+occurs. 2. When propionate is added to suspensions containing propan-2-ol, or if the suspensions are bubbled with CO2, a considerable uptake of K+occurs. 3. Maximum K+uptake occurs at a propionate concentration of 2mm. 4. The addition of 20mm-propionate to the suspension lowers the intracellular pH of the yeast from a resting value in the region of 6.2 to approx. 5.6. 5. When K+uptake is measured in the presence of 20mm-propionate, progressive changes in the rate of K+uptake and intracellular pH occur. The optimum rate of K+uptake occurs at an intracellular pH of 5.70. 6. The effect of both intra- and extra-cellular pH on K+–K+exchange was studied and an optimum rate was found at an extracellular pH of 5.35, the corresponding intracellular pH being 6.44. 7. When a Na+-loaded yeast oxidizes propan-2-ol in the presence of KCl, a steady efflux of Na+and influx of K+occurs. The addition of 10mm-propionate to the suspension markedly inhibited the Na+efflux but only slightly decreased the K+influx. 8. The effect of both extra- and intra-cellular pH on Na+efflux was studied with propan-2-ol and with glucose. The results can be best interpreted in terms of intracellular pH changes, and an optimum was obtained at approx. pH6.40.

scholarly journals The Role of the Primary Cilium in Sensing Extracellular pH

Cells ◽  
2019 ◽  
Vol 8 (7) ◽  
pp. 704 ◽  
Author(s):  
Kimberly F. Atkinson ◽  
Rinzhin T. Sherpa ◽  
Surya M. Nauli
Keyword(s):  
Endothelial Cells ◽  
Intracellular Ph ◽  
Primary Cilium ◽  
Primary Cilia ◽  
Extracellular Ph ◽  
Vascular Endothelial ◽  
Wild Type ◽  
Ph Changes ◽  
In Cells

Biosensors on the membrane of the vascular endothelium are responsible for sensing mechanical and chemical signals in the blood. Transduction of these stimuli into intracellular signaling cascades regulate cellular processes including ion transport, gene expression, cell proliferation, and/or cell death. The primary cilium is a well-known biosensor of shear stress but its role in sensing extracellular pH change has never been examined. As a cellular extension into the immediate microenvironment, the cilium could be a prospective sensor for changes in pH and regulator of acid response in cells. We aim to test our hypothesis that the primary cilium plays the role of an acid sensor in cells using vascular endothelial and embryonic fibroblast cells as in vitro models. We measure changes in cellular pH using pH-sensitive 2′,7′-biscarboxyethy1-5,6-carboxyfluorescein acetoxy-methylester (BCECF) fluorescence and mitogen-activated protein kinase (MAPK) activity to quantify responses to both extracellular pH (pHo) and intracellular pH (pHi) changes. Our studies show that changes in pHo affect pHi in both wild-type and cilia-less Tg737 cells and that the kinetics of the pHi response are similar in both cells. Acidic pHo or pHi was observed to change the length of primary cilia in wild-type cells while the cilia in Tg737 remained absent. Vascular endothelial cells respond to acidic pH through activation of ERK1/2 and p38-mediated signaling pathways. The cilia-less Tg737 cells exhibit delayed responsiveness to pHo dependent and independent pHi acidification as depicted in the phosphorylation profile of ERK1/2 and p38. Otherwise, intracellular pH homeostatic response to acidic pHo is similar between wild-type and Tg737 cells, indicating that the primary cilia may not be the sole sensor for physiological pH changes. These endothelial cells respond to pH changes with a predominantly K+-dependent pHi recovery mechanism, regardless of ciliary presence or absence.

The Role of Intracellular pH Changes in Heat Sensitization by Procaine

1993 ◽  
Vol 133 (1) ◽  
pp. 67 ◽  
Author(s):  
Eric D. Wieder ◽  
Michael H. Fox
Keyword(s):  
Intracellular Ph ◽  
Ph Changes ◽  
Heat Sensitization

scholarly journals The Effect of Extracellular pH Changes on Intracellular pH and Nitric Oxide Concentration in Endothelial and Smooth Muscle Cells from Rat Aorta

PLoS ONE ◽  
2013 ◽  
Vol 8 (5) ◽  
pp. e62887 ◽  
Author(s):  
Verena K. Capellini ◽  
Carolina B. A. Restini ◽  
Lusiane M. Bendhack ◽  
Paulo R. B. Evora ◽  
Andréa C. Celotto
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Intracellular Ph ◽  
Muscle Cells ◽  
Rat Aorta ◽  
Extracellular Ph ◽  
Ph Changes ◽  
Oxide Concentration ◽  
Nitric Oxide Concentration

scholarly journals Intracellular Acidification Causes Adenosine Release During States of Hyperexcitability in the Hippocampus

2009 ◽  
Vol 102 (3) ◽  
pp. 1984-1993 ◽  
Author(s):  
Chris G. Dulla ◽  
Bruno G. Frenguelli ◽  
Kevin J. Staley ◽  
Susan A. Masino
Keyword(s):  
Synaptic Transmission ◽  
Intracellular Ph ◽  
Hippocampal Slice ◽  
Dominant Role ◽  
Hippocampal Slices ◽  
Extracellular Ph ◽  
Ph Change ◽  
Extracellular Adenosine ◽  
Adenosine Concentration

Decreased pH increases extracellular adenosine in CNS regions as diverse as hippocampus and ventral medulla. However, thus far there is no clear consensus whether the critical pH change is a decrease in intracellular and/or extracellular pH. Previously we showed that a decrease in extracellular pH is necessary and a decrease in intracellular pH alone is not sufficient, to increase extracellular adenosine in an acute hippocampal slice preparation. Here we explored further the role of intracellular pH under different synaptic conditions in the hippocampal slice. When synaptic excitability was increased, either during γ-aminobutyric acid type A receptor blockade in CA1 or after the induction of persistent bursting in CA3, a decrease in intracellular pH alone was now sufficient to: 1) elevate extracellular adenosine concentration, 2) activate adenosine A1 receptors, 3) decrease excitatory synaptic transmission (CA1), and 4) attenuate burst frequency in an in vitro seizure model (CA3). Hippocampal slices obtained from adenosine A1 receptor knockout mice did not exhibit these pH-mediated effects on synaptic transmission, further confirming the role of adenosine acting at the adenosine A1 receptor. Taken together, these data strengthen and add significantly to the evidence outlining a change in pH as an important stimulus influencing extracellular adenosine. In addition, we identify conditions under which intracellular pH plays a dominant role in regulating extracellular adenosine concentrations.

scholarly journals Atrial Natriuretic Peptide Effects on Intracellular pH Changes and ROS Production in HEPG2 Cells: Role of p38 MAPK and Phospholipase D

2005 ◽  
Vol 15 (1-4) ◽  
pp. 077-088 ◽  
Author(s):  
Patrizia Baldini ◽  
Paolo De Vito ◽  
Daniela Vismara ◽  
Claudia Bagni ◽  
Francesca Zalfa ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
P38 Mapk ◽  
Intracellular Ph ◽  
Natriuretic Peptide ◽  
Phospholipase D ◽  
Hepg2 Cells ◽  
Ros Production ◽  
Ph Changes ◽  
Atrial Natriuretic

Modulatory effects of acid-sensing ion channels on action potential generation in hippocampal neurons

2004 ◽  
Vol 287 (3) ◽  
pp. C682-C690 ◽  
Author(s):  
Marija Vukicevic ◽  
Stephan Kellenberger
Keyword(s):  
Ion Channels ◽  
Hippocampal Neurons ◽  
Extracellular Ph ◽  
Ph Changes ◽  
Acid Sensing Ion Channels ◽  
Close Proximity ◽  
First Time ◽  
Rapid Drop ◽  
Cultured Hippocampal Neurons

Extracellular acidification has been shown to generate action potentials (APs) in several types of neurons. In this study, we investigated the role of acid-sensing ion channels (ASICs) in acid-induced AP generation in brain neurons. ASICs are neuronal Na+ channels that belong to the epithelial Na+ channel/degenerin family and are transiently activated by a rapid drop in extracellular pH. We compared the pharmacological and biophysical properties of acid-induced AP generation with those of ASIC currents in cultured hippocampal neurons. Our results show that acid-induced AP generation in these neurons is essentially due to ASIC activation. We demonstrate for the first time that the probability of inducing APs correlates with current entry through ASICs. We also show that ASIC activation in combination with other excitatory stimuli can either facilitate AP generation or inhibit AP bursts, depending on the conditions. ASIC-mediated generation and modulation of APs can be induced by extracellular pH changes from 7.4 to slightly <7. Such local extracellular pH values may be reached by pH fluctuations due to normal neuronal activity. Furthermore, in the plasma membrane, ASICs are localized in close proximity to voltage-gated Na+ and K+ channels, providing the conditions necessary for the transduction of local pH changes into electrical signals.

Effects of bicarbonate and pH on chloride transport by gastric mucosa

1982 ◽  
Vol 243 (1) ◽  
pp. G60-G68 ◽  
Author(s):  
E. C. Manning ◽  
T. E. Machen
Keyword(s):  
Gastric Mucosa ◽  
Intracellular Ph ◽  
Chloride Transport ◽  
Short Circuit ◽  
Ph Dependence ◽  
Short Circuit Current ◽  
Extracellular Ph ◽  
Solution Ph ◽  
Ph Changes

HCO3 and pH dependence of net Cl transport (JClnet) by resting (metiamide-treated) frog gastric mucosa has been investigated in vitro by measuring short-circuit current (Isc = JClnet) and transepithelial conductance (G). With either 100% O2 or 95% O2-5% CO2 gassing, HCO3-free solutions caused large (greater than 50%) reductions in Isc and G. Increases in [HCO3] of the serosal, but not mucosal, solution caused increases in Isc and G. At least part of the effect appeared to be due specifically to the HCO3 moiety, as opposed to the pH changes that also occurred. In HCO3-free solutions (100% O2), increasing serosal solution pH above 7 with either permeable or impermeable buffers caused Isc and G to increase; permeable buffers were somewhat more effective than impermeable buffers. Measurements of intracellular pH (pHc) with [14C]DMO or [14C]methylamine showed that increases in extracellular pH (pHo) caused increases in cellular pH (pHc), and these changes in pHc were independent of buffer type. We conclude that HCO3 and/or high pHo stimulate Isc and G and that buffer permeability and cellular concentration can also affect transport.

scholarly journals Intracellular pH modulates the availability of vascular L-type Ca2+ channels.

1994 ◽  
Vol 103 (4) ◽  
pp. 647-663 ◽  
Author(s):  
U Klöckner ◽  
G Isenberg
Keyword(s):  
Intracellular Ph ◽  
Single Channel ◽  
Surface Membrane ◽  
Life Time ◽  
Bicarbonate Buffer ◽  
State Changes ◽  
Channel Currents ◽  
Inside Out ◽  
Ca2 Channels

L-type Ca2+ channel currents were recorded from myocytes isolated from bovine pial and porcine coronary arteries to study the influence of changes in intracellular pH (pHi). Whole cell ICa fell when pHi was made more acidic by substituting HEPES/NaOH with CO2/bicarbonate buffer (pHo 7.4, 36 degrees C), and increased when pHi was made more alkaline by addition of 20 mM NH4Cl. Peak ICa was less pHi sensitive than late ICa (170 ms after depolarization to 0 mV). pHi-effects on single Ca2+ channel currents were studied with 110 mM BaCl2 as the charge carrier (22 degrees C, pHo 7.4). In cell-attached patches pHi was changed by extracellular NH4Cl or through the opened cell. In inside-out patches pHi was controlled through the bath. Independent of the method used the following results were obtained: (a) Single channel conductance (24 pS) and life time of the open state were not influenced by pHi (between pHi 6 and 8.4). (b) Alkaline pHi increased and acidic pHi reduced the channel availability (frequency of nonblank sweeps). (c) Alkaline pHi increased and acidic pHi reduced the frequency of late channel re-openings. The effects are discussed in terms of a deprotonation (protonation) of cytosolic binding sites that favor (prevent) the shift of the channels from a sleepy to an available state. Changes of bath pHo mimicked the pHi effects within 20 s, suggesting that protons can rapidly permeate through the surface membrane of vascular smooth muscle cells. The role of pHi in Ca2+ homeostases and vasotonus is discussed.

scholarly journals Cytoplasmic [Ca2+] and intracellular pH in lymphocytes. Role of membrane potential and volume-activated Na+/H+ exchange.

1987 ◽  
Vol 89 (2) ◽  
pp. 185-213 ◽  
Author(s):  
S Grinstein ◽  
S Cohen
Keyword(s):  
Protein Kinase C ◽  
Membrane Potential ◽  
Protein Kinase ◽  
Intracellular Ph ◽  
Enzyme Treatment ◽  
Membrane Hyperpolarization ◽  
Kinase C ◽  
Free Media ◽  
Stimulation Of

The effect of elevating cytoplasmic Ca2+ [( Ca2+]i) on the intracellular pH (pHi) of thymic lymphocytes was investigated. In Na+-containing media, treatment of the cells with ionomycin, a divalent cation ionophore, induced a moderate cytoplasmic alkalinization. In the presence of amiloride or in Na+-free media, an acidification was observed. This acidification is at least partly due to H+ (equivalent) uptake in response to membrane hyperpolarization since: it was enhanced by pretreatment with conductive protonophores, it could be mimicked by valinomycin, and it was decreased by depolarization with K+ or gramicidin. In addition, activation of metabolic H+ production also contributes to the acidification. The alkalinization is due to Na+/H+ exchange inasmuch as it is Na+ dependent, amiloride sensitive, and accompanied by H+ efflux and net Na+ gain. A shift in the pHi dependence underlies the activation of the antiport. The effect of [Ca2+]i on Na+/H+ exchange was not associated with redistribution of protein kinase C and was also observed in cells previously depleted of this enzyme. Treatment with ionomycin induced significant cell shrinking. Prevention of shrinking largely eliminated the activation of the antiport. Moreover, a comparable shrinking produced by hypertonic media also activated the antiport. It is concluded that stimulation of Na+/H+ exchange by elevation of [Ca2+]i is due, at least in part, to cell shrinking and does not require stimulation of protein kinase C.

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