Cell membrane potential: a signal to control intracellular pH and transepithelial hydrogen ion secretion in frog kidney

1987 ◽  
Vol 409 (3) ◽  
pp. 289-295 ◽  
Author(s):  
W. Wang ◽  
P. Dietl ◽  
S. Silbernagl ◽  
H. Oberleithner
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Intracellular Ph ◽  
Cell Membrane Potential ◽  
Hydrogen Ion ◽  
Frog Kidney ◽  
Ion Secretion

scholarly journals Intracellular pH regulation in freshly isolated suspensions of rabbit inner medullary collecting duct cells: role of Na+:H+ antiporter and H(+)-ATPase.

1990 ◽  
Vol 1 (6) ◽  
pp. 890-901
Author(s):  
D Kikeri ◽  
M L Zeidel
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Intracellular Ph ◽  
Recovery Rate ◽  
Collecting Duct ◽  
Atp Depletion ◽  
Cell Membrane Potential ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct ◽  
In Cells

To define proton transport mechanisms involved in the regulation of intracellular pH (pHi) in cells of the inner medullary collecting duct (IMCD), pHi and cell membrane potential were estimated by using the fluorescent dyes 2,7-biscarboxyethyl-5(6)-carboxyfluorescein and 3,3'-dipropylthiadicarbocyanine iodide, respectively, in suspensions of freshly isolated rabbit IMCD cells. The resting pHi of IMCD cells in nonbicarbonate Ringer's solution (pH 7.4) was 7.21 +/- 0.03 (mean +/- SE). When cells were acidified by ammonium withdrawal, the initial pHi recovery rate was 0.33 +/- 0.02 pH unit/min; replacement of extracellular Na+ (130 mM) with N-methyl-D-glucamine+ reduced the pHi recovery rate to 0.08 +/- 0.02 pH unit/min, while addition of 0.1 mM amiloride in the presence of extracellular Na+ reduced the rate of pHi recovery to 0.02 +/- 0.02 pH unit/min. Similar results were obtained in cells acid loaded with HCl. Cells recovering from acidification exhibited 22Na+ uptake rates threefold higher than did nonacidified cells. The rate of Na(+)-dependent pHi recovery was independent of the cell membrane potential. In the absence of extracellular Na+, depolarizing cell membrane potential in a stepwise manner by increasing extracellular K+ concentrations from 1 to 130 mM resulted in graded increments in the rate of pHi recovery. In the presence of 130 mM K+, the pHi recovery rate in acidified cells was dependent on cellular ATP levels, sensitive to 1 mM N-ethylmaleimide, and insensitive to 0.01 mM oligomycin in the presence of glucose (control, 0.24 +/- 0.01; ATP-depleted, 0.13 +/- 0.02; addition of N-ethylmaleimide, 0.16 +/- 0.01; addition of oligomycin, 0.27 +/- 0.02 pH unit/min). ATP depletion markedly inhibited H+ extrusion from IMCD cells measured by using a pH stat. These results provide direct evidence in freshly isolated IMCD cells that both a Na+:H+ antiporter and a rheogenic H(+)-ATPase participate in pHi regulation.

scholarly journals Modulation of calcium fluxes in Jurkat T cells by myristic acid. Inhibition is independent of membrane potential and intracellular pH

1992 ◽  
Vol 283 (1) ◽  
pp. 113-118 ◽  
Author(s):  
T Nordström ◽  
T Mustelin ◽  
T Pessa-Morikawa ◽  
L C Andersson
Keyword(s):  
T Cells ◽  
Membrane Potential ◽  
T Cell ◽  
Cell Membrane ◽  
Intracellular Ph ◽  
Myristic Acid ◽  
Blocking Effect ◽  
Cell Membrane Potential ◽  
Jurkat Cells ◽  
Jurkat T Cells

Treatment of T lymphocytes with mitogenic antibodies against the T-cell receptor/CD3 complex induces within seconds a rise in the concentration of intracellular free Ca2+. We recently reported that free myristic acid, but not its methyl ester, inhibits both the anti-CD3-induced Ca2+ influx across the cell membrane and the Ca2+ release from intracellular stores in Jurkat T cells. Here we show that myristic acid induced a rapid hyperpolarization of the cell membrane potential and a decrease in intracellular pH in Jurkat cells. Lauric acid and palmitic acid caused minor hyperpolarization, whereas other saturated non-esterified fatty acids tested were without effect. Hyperpolarization of the membrane potential in Jurkat cells with valinomycin did not, however, inhibit the anti-CD3-induced Ca2+ signal, and the blocking effect on the Ca2+ signal in myristic acid-treated Jurkat cells was not reversed after normalization of the cell membrane potential by treatment with gramicidin. The inhibitory effect of myristic acid on the Ca2+ fluxes thus cannot be explained by changes in membrane potential. We also present evidence that the blocking effect of myristic acid on the receptor-operated Ca2+ flux is not due to the myristic acid-induced decrease in intracellular pH. Moreover, we demonstrate that myristic acid does not prevent the release of Ca2+ triggered by inositol 1,4,5-trisphosphate from intracellular pools in permeabilized cells. Our findings indicate that myristic acid blocks anti-CD3-induced Ca2+ traffic in Jurkat cells by interfering with the regulation of Ca2+ mobilization, apparently by blocking an early step in signal transduction from the T-cell-antigen receptor/CD3 complex.

Pressure-induced smooth muscle cell depolarization in pulmonary arteries from control and chronically hypoxic rats does not cause myogenic vasoconstriction

2005 ◽  
Vol 98 (3) ◽  
pp. 1119-1124 ◽  
Author(s):  
Jay S. Naik ◽  
Scott Earley ◽  
Thomas C. Resta ◽  
Benjimen R. Walker
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Cell Membrane ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arteries ◽  
Barometric Pressure ◽  
Cell Membrane Potential ◽  
Intraluminal Pressure ◽  
Dose Dependent

Chronic obstructive pulmonary diseases, as well as prolonged residence at high altitude, can result in generalized airway hypoxia, eliciting an increase in pulmonary vascular resistance. We hypothesized that a portion of the elevated pulmonary vascular resistance following chronic hypoxia (CH) is due to the development of myogenic tone. Isolated, pressurized small pulmonary arteries from control (barometric pressure ≅ 630 Torr) and CH (4 wk, barometric pressure = 380 Torr) rats were loaded with fura 2-AM and perfused with warm (37°C), aerated (21% O2-6% CO2-balance N2) physiological saline solution. Vascular smooth muscle (VSM) intracellular Ca2+ concentration ([Ca2+]i) and diameter responses to increasing intraluminal pressure were determined. Diameter and VSM cell [Ca2+]i responses to KCl were also determined. In a separate set of experiments, VSM cell membrane potential responses to increasing luminal pressure were determined in arteries from control and CH rats. VSM cell membrane potential in arteries from CH animals was depolarized relative to control at each pressure step. VSM cells from both groups exhibited a further depolarization in response to step increases in intraluminal pressure. However, arteries from both control and CH rats distended passively to increasing intraluminal pressure, and VSM cell [Ca2+]i was not affected. KCl elicited a dose-dependent vasoconstriction that was nearly identical between control and CH groups. Whereas KCl administration resulted in a dose-dependent increase in VSM cell [Ca2+]i in arteries taken from control animals, this stimulus elicited only a slight increase in VSM cell [Ca2+]i in arteries from CH animals. We conclude that the pulmonary circulation of the rat does not demonstrate pressure-induced vasoconstriction.

Ammonia movement and distribution after exercise across white muscle cell membranes in rainbow trout

1996 ◽  
Vol 271 (3) ◽  
pp. R738-R750 ◽  
Author(s):  
Y. Wang ◽  
G. J. Heigenhauser ◽  
C. M. Wood
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Intracellular Ph ◽  
Muscle Cell ◽  
Cell Membranes ◽  
White Muscle ◽  
Extracellular Ph ◽  
Posterior Portion ◽  
Arterial Inflow ◽  
Muscle Cell Membrane

Manipulations of pH and electrical gradients in a perfused preparation were used to analyze the factors controlling ammonia distribution and flux in trout white muscle after exercise. Trout were exercised to exhaustion, and then an isolated-perfused white muscle preparation with discrete arterial inflow and venous outflow was made from the posterior portion of the tail. The tail-trunks were perfused with low (7.4)-, medium (7.9)-, and high (8.4)-pH saline, achieved by varying HCO3- concentration ([HCO3-]) at constant Pco2. Intracellular and extracellular pH, ammonia, CO2, K+, Na+, and Cl- were measured. Muscle intracellular pH was not affected by changes in extracellular pH. Increasing extracellular pH caused a decrease in the transmembrane NH3 partial pressure (PNH3) gradient and a decrease in ammonia efflux. When extracellular K+ concentration was increased from 3.5 to 15 mM in the medium-pH group, a depolarization of the muscle cell membrane potential from -92 to -60 mV and a 0.1-unit depression in intracellular pH occurred. Ammonia efflux increased despite a marked reduction in the PNH3 gradient. Amiloride (10(-4) M) had no effect, indicating that Na+/H(+)-NH4+ exchange does not participate in ammonia transport in this system. A comparison of observed intracellular-to-extracellular ammonia distribution ratios with those modeled according to either pH or Nernst potential distributions supports a model in which ammonia distribution across white muscle cell membranes is affected by both pH and electrical gradients, indicating that the membranes are permeable to both NH3 and NH4+. Membrane potential, acting to retain high levels of NH4+ in the intracellular compartment, appears to have the dominant influence during the postexercise period. However, at rest, the pH gradient may be more important, resulting in much lower intracellular ammonia levels and distribution ratios. We speculate that the muscle cell membrane NH3-to-NH4+ permeability ratio in trout may change between the rest and postexercise condition.

Cell Membrane Potential Model Circuit Lab

2018 ◽  
Vol 56 (8) ◽  
pp. 540-543
Author(s):  
Mickey D. Kutzner ◽  
J. Michael Bryson
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Potential Model ◽  
Cell Membrane Potential ◽  
Model Circuit

scholarly journals Signaling mechanism by the Staphylococcus aureus two-component system LytSR: role of acetyl phosphate in bypassing the cell membrane electrical potential sensor LytS

F1000Research ◽  
2016 ◽  
Vol 4 ◽  
pp. 79 ◽  
Author(s):  
Kevin Patel ◽  
Dasantila Golemi-Kotra
Keyword(s):  
Staphylococcus Aureus ◽  
Membrane Potential ◽  
Cell Membrane ◽  
Electrical Potential ◽  
Cell Membrane Potential ◽  
Acetyl Phosphate ◽  
Two Component System ◽  
Component System ◽  
Two Component ◽  
Membrane Electrical Potential

The two-component system LytSR has been linked to the signal transduction of cell membrane electrical potential perturbation and is involved in the adaptation of Staphylococcus aureus to cationic antimicrobial peptides. It consists of a membrane-bound histidine kinase, LytS, which belongs to the family of multiple transmembrane-spanning domains receptors, and a response regulator, LytR, which belongs to the novel family of non-helix-turn-helix DNA-binding domain proteins. LytR regulates the expression of cidABC and lrgAB operons, the gene products of which are involved in programmed cell death and lysis. In vivo studies have demonstrated involvement of two overlapping regulatory networks in regulating the lrgAB operon, both depending on LytR. One regulatory network responds to glucose metabolism and the other responds to changes in the cell membrane potential. Herein, we show that LytS has autokinase activity and can catalyze a fast phosphotransfer reaction, with 50% of its phosphoryl group lost within 1 minute of incubation with LytR. LytS has also phosphatase activity. Notably, LytR undergoes phosphorylation by acetyl phosphate at a rate that is 2-fold faster than the phosphorylation by LytS. This observation is significant in lieu of the in vivo observations that regulation of the lrgAB operon is LytR-dependent in the presence of excess glucose in the medium. The latter condition does not lead to perturbation of the cell membrane potential but rather to the accumulation of acetate in the cell. Our study provides insights into the molecular basis for regulation of lrgAB in a LytR-dependent manner under conditions that do not involve sensing by LytS.

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