Heat-Induced Changes in Intracellular Sodium and Membrane Potential: Lack of a Role in Cell Killing and Thermotolerance

1996 ◽  
Vol 146 (3) ◽  
pp. 283 ◽  
Author(s):  
George P. Amorino ◽  
Michael H. Fox
Keyword(s):  
Membrane Potential ◽  
Cell Killing ◽  
Intracellular Sodium ◽  
Induced Changes

scholarly journals Concanavalin A causes an increase in sodium permeability and intracellular sodium content of pig lymphocytes

1983 ◽  
Vol 210 (3) ◽  
pp. 893-897 ◽  
Author(s):  
S M Felber ◽  
M D Brand
Keyword(s):  
Plasma Membrane ◽  
Membrane Potential ◽  
Concanavalin A ◽  
Permeability Coefficient ◽  
Sodium Content ◽  
Intracellular Sodium ◽  
Resting Cells ◽  
Sodium Permeability ◽  
Induced Changes ◽  
Stimulation Of

1. The 3mV depolarization of pig lymphocytes observed within 2 1/2 min of treatment with concanavalin A [Felber & Brand (1983) Biochem. J. 210, 885-891] is dependent on the presence of high extracellular [Na+]. 2. The concanavalin A-induced changes in membrane potential at high and low extracellular [Na+] are quantitatively explained by an increase in the electrogenic permeability coefficient for Na+ (PNa). This rises from a negligible value in resting cells to around 4% of the permeability coefficient for K+ or Cl- in stimulated cells. 3. Concanavalin A induces a 4mM increase in the Na+ content of pig lymphocytes. This increase in intracellular [Na+] is not due solely to stimulation of electrogenic Na+ influx resulting from the rise in PNa. 4. Thus concanavalin A stimulates both an electrogenic pathway for Na+ influx, resulting in a small depolarization of the plasma membrane, and a non-electrogenic Na+ influx pathway, resulting in a rise in intracellular [Na+].

scholarly journals Ionomycin-Induced Changes in Membrane Potential Alter Electroporation Outcomes in HL-60 Cells

2018 ◽  
Vol 114 (12) ◽  
pp. 2875-2886 ◽  
Author(s):  
Erik J. Aiken ◽  
Brian G. Kilberg ◽  
Siyuan Yu ◽  
Susan C. Hagness ◽  
John H. Booske
Keyword(s):  
Membrane Potential ◽  
Induced Changes

Low doses of ethanol have Ca2+ ionophore-like effects on apical membrane potential of in vitro Necturus antrum

1991 ◽  
Vol 261 (1) ◽  
pp. G92-G103
Author(s):  
M. J. Rutten ◽  
C. D. Moore
Keyword(s):  
Membrane Potential ◽  
Apical Membrane ◽  
Periodic Acid ◽  
Ethanol Exposure ◽  
Membrane Potentials ◽  
Antral Mucosa ◽  
Low Doses ◽  
Periodic Acid Schiff ◽  
Induced Changes

The effects of low doses of luminal ethanol on the amiloride-sensitive apical membrane potential of Necturus antral mucosa were studied using conventional microelectrode techniques. Luminal ethanol (0.250-4.0% vol/vol) caused a dose-dependent hyperpolarization of the apical membrane potential (Vmc), an increase in transepithelial resistance (Rt) and resistance ratio (Ra/Rb), and a decrease in transepithelial potential (Vms). Luminal amiloride (100 microM) to 4% ethanol-treated antra did not cause any additional hyperpolarization of Vmc. Compared with luminal 2% ethanol-Ringer, an equivalent osmotic mannitol solution depolarized Vmc and basolateral potential (Vcs), decreased Rt and Ra/Rb, and increased Vms. A single dose of 0.50% ethanol attenuated the effects of a second 2% ethanol exposure on Vmc. No change in periodic acid-Schiff (PAS)-positive mucous granule content could be found between control and 2% ethanol-treated antra. The Ca2+ ionophores A23187 or ionomycin (0.25-5.0 microM) dose dependently hyperpolarized the Vmc and Vcs, increased Rt and Ra/Rb, and decreased Vms. Luminal Ca(2+)-free Ringer had no effect on luminal 2.00% ethanol-induced changes in membrane potentials or resistances. Pretreatment with BAPTA blocked by approximately 70 and 55% the Vmc hyperpolarization of 2 and 4% ethanol, respectively. Pretreatment with ruthenium red (10-50 microM) also dose dependently reduced the 2% ethanol-induced changes in Vmc. The data indicate that 1) low doses of luminal ethanol and Ca2+ ionophores have similar effects on Necturus gastric antral membrane potentials and resistances, 2) ethanol-induced hyperpolarizations of the Vmc are partially mediated through an alteration in intracellular Ca2+, and 3) low doses of luminal ethanol do not cause the release of antral epithelial mucous granules at the time when significant changes are occurring in the Vmc.

Mapping of capillary flow, cellular redox state, and resting membrane potential in hypoperfused rat myocardium

1999 ◽  
Vol 277 (5) ◽  
pp. H2050-H2064 ◽  
Author(s):  
Frank Brasch ◽  
Marion Neckel ◽  
Rolf Volkmann ◽  
Gerhard Schmidt ◽  
Gerhard Hellige ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Trypan Blue ◽  
Redox State ◽  
Capillary Flow ◽  
Resting Membrane Potential ◽  
Capillary Perfusion ◽  
Cellular Redox ◽  
Nadh Fluorescence ◽  
Induced Changes ◽  
Tetramethylrhodamine Methyl Ester

The influence on myocyte viability of ischemia-induced changes in capillary perfusion was studied in the hearts of anesthetized rats subjected to partial occlusion of the left coronary artery for 45 min. Timed plasma labeling was applied to determine perfusion patterns. Changes in the fluorescence of preloaded potential-sensitive dyes [tetramethylrhodamine methyl ester (TMRM) and bis-oxonol], of trypan blue, and of endogeneous NADH were utilized in characterizing myocyte viability in histological sections of the heart. Within the hypoperfused zone, localized areas appeared vascularly nonlabeled for periods of at least 10 min. Within these areas a reduction in TMRM fluorescence occurred in 82.5% of the tissue, signaling a reduced resting membrane potential. In the same areas 37.7% of the myocytes revealed an NADH fluorescence lower than that regularly found in anoxic tissues. This correlated with an especially low level of TMRM, with increased fluorescence bis-oxonol and with an accumulation of trypan blue. In conclusion, in localized hypoperfusion-induced zones lacking capillary flow, an inhomogeneous pattern of reductions in myocyte viability develops, which appears to be relevant in ischemia-induced arrhythmias.

Intracellular sodium ion activity: reliable measurement and stimulation-induced change in cardiac Purkinje fibers

1987 ◽  
Vol 65 (5) ◽  
pp. 954-962 ◽  
Author(s):  
Chin O. Lee ◽  
Wook B. Im ◽  
Jong K. Sonn
Keyword(s):  
Membrane Potential ◽  
Time Constant ◽  
Fast Response ◽  
Intracellular Sodium ◽  
Sodium Ion ◽  
Sodium Influx ◽  
Stimulation Rate ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers ◽  
Ion Activity

Recently Na+-selective microelectrodes (NaSM) have been used to measure quantitatively small changes in intracellular sodium ion activity [Formula: see text] and to determine a precise time course of comparatively rapid change in [Formula: see text]. In such studies, accurate measurement of [Formula: see text] requires the following criteria: (i) NaSM should have a fast response time and (ii) an NaSM and a conventional voltage microelectrode should measure the same membrane potential. These criteria were evaluated by measuring [Formula: see text] when membrane potential of cardiac Purkinje fibers was suddenly hyperpolarized and depolarized by changing stimulation rate. The NaSM coated with a conductive silver paint had fast response times so that rapid changes in [Formula: see text] could be reliably measured. The cardiac Purkinje fibers stimulated at a constant rate generated uniform membrane voltage and the NaSM and conventional microelectrode measured virtually the same membrane potential. This result is somewhat different from that reported under voltage-clamp condition by other investigators. The [Formula: see text] of the fibers increased as the stimulation rate was increased over the range of 0.5–3 Hz. In fibers stimulated at 1 Hz, cessation of stimulation was immediately followed by an exponential decline of [Formula: see text] with an average time constant of 53 ± 9 s (SD, n = 8), or rate constant of 0.020 ± 0.004/s. Restimulation of the fibers produced an exponential rise of [Formula: see text] with an average time constant of 65 ± 12 s (n = 8). Similar results were obtained in fibers stimulated at 2 Hz. The average rates of rise of [Formula: see text] after the onset of stimulations at 1 and 2 Hz were 1.0 and 1.5 mM/min, equivalent to increments in net sodium influx of 13.2 and 19.8 pmol∙cm−2∙s−1, respectively. The average maximum rate of [Formula: see text] rise produced by the application of 10−5 M strophanthidin to the fibers stimulated at 1 Hz was 1.3 ± 0.5 mM/min, equivalent to a net sodium influx of 17.2 pmol∙cm−2∙s−1.

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