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 Early plasma-membrane-potential changes during stimulation of lymphocytes by concanavalin A.

1983 ◽  
Vol 210 (3) ◽  
pp. 885-891 ◽  
Author(s):  
S M Felber ◽  
M D Brand
Keyword(s):  
Plasma Membrane ◽  
Membrane Potential ◽  
Concanavalin A ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
K Channel ◽  
Ionophore A23187 ◽  
Resting Cells ◽  
Plasma Membrane Potential ◽  
Stimulation Of

1. We have monitored the plasma-membrane potential of lymphocytes by measuring the accumulation of the lipophilic cation methyltriphenylphosphonium (TPMP+) in the presence of the uncoupler carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP). 2. The mitogen concanavalin A causes a decrease in TPMP+ accumulation by pig lymphocytes corresponding to a 3 mV depolarization with 2 1/2 min. Concanavalin A does not alter 86Rb+ uptake in the first 30 min. 3. In contrast concanavalin A increased TPMP+ accumulation and the rate of Rb+ uptake in mouse thymocytes. This is consistent with a previous proposal that the mitogen induces a hyperpolarization of mouse thymocytes as a result of stimulation of a Ca2+-dependent K+ channel. 4. Studies with the calcium ionophore A23187 and quinine (an inhibitor of the Ca2+-dependent K+ channel) suggest that the channel is partially closed in mouse resting thymocytes but is almost fully active in pig resting cells. Thus concanavalin A hyperpolarizes mouse thymocytes by activating the Ca2+-dependent K+ channel but cannot do so in pig lymphocytes because the channel is already maximally activated. 5. The 3mV depolarization of pig cells cannot be explained by a decrease in electrogenic K+ permeability.

Mechanismus der cis- und trans-Stimulierung der Anionenfluxe durch die Plasmamembran der Pflanzenzelle / Mechanism of Cis- and Trans-Stimulation of Anion Fluxes across the Plasma Membrane of Plant Cells

1970 ◽  
Vol 25 (6) ◽  
pp. 631-636 ◽  
Author(s):  
Josef Weigl
Keyword(s):  
Plasma Membrane ◽  
Permeability Coefficient ◽  
Electrical Potential ◽  
Plant Cells ◽  
Monovalent Cations ◽  
Trans Effect ◽  
Anion Permeation ◽  
Ion Efflux ◽  
Cis And Trans ◽  
Stimulation Of

Trans-stimulation by salts of the passive efflux of Cl⊖ across the plasma membrane of plant cells was established previously. In this paper the trans-effect of salts is compared with the effect of nystatin on ion efflux. It is further shown that the influx of anions is also stimulated by external salts. Influx of Cl⊖ was stimulated by K2SO4 (>~1 mM), influx of SO42⊖ was stimulated by KCl (>~lmM). This suggests that with increasing external salt concentration not only the electrical potential across the plasmalemma is lowered (due to preferential permeability to monovalent cations) but alsoth e permeability (i. e. the permeability coefficient) of the plasmalemma to anions is increased. According to the model proposed for the salt-stimulated decrease in the resistance to passive anion permeation the plasmalemma may be considered a lipid lattice-electrofilter. The nature of the coupling of the counter fluxes is discussed.

scholarly journals Sodium and calcium interactions in vascular smooth muscle cells of the rabbit ear artery.

1979 ◽  
Vol 74 (1) ◽  
pp. 57-70 ◽  
Author(s):  
G Droogmans ◽  
R Casteels
Keyword(s):  
Plasma Membrane ◽  
Membrane Potential ◽  
Efflux Rate ◽  
Rabbit Ear Artery ◽  
Tension Development ◽  
Ear Artery ◽  
Rabbit Ear ◽  
Exchange Hypothesis ◽  
45Ca Efflux ◽  
Stimulation Of

The effects of Na-free and of K-free solutions on the membrane potential, on tension development, and on 45Ca exchange have been investigated in rabbit ear artery. The contraction induced by Na-free solutions and the tension which develops in K-free solutions after a delay of about 1 h are both submaximal. Exposure for 4 h to K-free solutions does not affect the membrane potential, whereas Na-free solutions depolarize the cells by 10-20 mV, depending on the Na-substitute. Neither the amplitude nor the rate constant of the slowly exchanging 45Ca-fraction is affected by these experimental procedures. Substituting external Na by choline or TMA induces a transient increase of the 45Ca-efflux rate which does not occur in a Ca-free efflux medium, and which can be blocked with La. K readmission to Na-enriched tissues hyperpolarizes the cells up to -100 mV and induces a relaxation, without exerting any effect on the 45Ca efflux rate. The release of Ca from intracellular stores, induced by histamine and FCCP, and its subsequent extrusion through the plasma membrane produce a transient stimulation of the 45Ca efflux, which is not affected by the reduction of the Na gradient. The transient contraction induced by histamine in Ca-free solutions is affected in a different way by different Na substitutes. The results do not fit the Na-Ca exchange hypothesis but are consistent with an effect of the Na gradient on the passive Ca influx.

scholarly journals Factors determining the plasma-membrane potential of lymphocytes

1982 ◽  
Vol 204 (2) ◽  
pp. 577-585 ◽  
Author(s):  
S M Felber ◽  
M D Brand
Keyword(s):  
Plasma Membrane ◽  
Membrane Potential ◽  
Permeability Coefficient ◽  
Culture Medium ◽  
Low Permeability ◽  
Plasma Membrane Potential ◽  
Normal Culture ◽  
Mesenteric Lymph ◽  
Carbonyl Cyanide ◽  
Set Up

1. Lymphocytes from pig mesenteric lymph node have low permeability to K+ (Rb+), Na+ and Cl-. None of these ions is in Nernst equilibrium with the plasma-membrane potential (delta psi p). 2. delta psi p can be calculated from the transmembrane distribution of the permeant cation methyltriphenylphosphonium (TPMP+) in the presence of the uncoupler carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP) to abolish uptake into intracellular mitochondria. In normal culture medium delta psi p is 56 mV. 3. A similar potential is found in T-enriched pig cells and in mouse thymocytes. 4. The contribution of electrogenic (Na+ + K+)ATPase to delta psi p is about 7 mV. 5. The remainder of the lymphocyte delta psi p is a polyionic potential set up by K+ and Cl- with a permeability coefficient for Cl- of similar magnitude to that for K+.

Alanine stimulation of passive potassium efflux in hepatocytes is independent of Na(+)-K+ pump activity

1990 ◽  
Vol 258 (1) ◽  
pp. C24-C29 ◽  
Author(s):  
B. J. Cohen ◽  
C. Lechene
Keyword(s):  
Initial Rate ◽  
Rat Hepatocytes ◽  
Sodium Content ◽  
Intracellular Sodium ◽  
Cell Swelling ◽  
Hypotonic Solution ◽  
Potassium Efflux ◽  
Pump Rate ◽  
Pump Activity ◽  
Stimulation Of

We have studied the effects of alanine on electrolyte content and ion transport in rat hepatocytes in primary culture. Application of 10 mM alanine is followed by 1) an increase in the rate of sodium entry; 2) an increase in intracellular sodium content; 3) an increase in ouabain-inhibitable rubidium uptake, a measure of Na(+)-K+ pump rate; 4) an increase in unidirectional potassium efflux, whether or not the Na(+)-K+ pump was inhibited; and 5) an increase in the initial rate of potassium loss after Na(+)-K+ pump inhibition. This increase occurred even when alanine was presented in Ringer made hypertonic by the addition of sucrose. Application of hypotonic solution led to a significant net loss of potassium, but no net loss of potassium was observed after alanine application. Thus alanine stimulates the Na(+)-K+ pump by increasing intracellular sodium secondary to an increase in the rate of sodium entry. Passive potassium efflux is stimulated by a mechanism that is independent of the stimulation of the Na(+)-K+ pump. The stimulated potassium efflux does not appear to be a response to cell swelling.

scholarly journals Electrogenic H+ pathway contributes to stimulus-induced changes of internal pH and membrane potential in intact neutrophils: role of cytoplasmic phospholipase A2

1997 ◽  
Vol 325 (2) ◽  
pp. 501-510 ◽  
Author(s):  
Katalin SUSZTÁK ◽  
Attila MÓCSAI ◽  
Erzsébet LIGETI ◽  
András KAPUS
Keyword(s):  
Membrane Potential ◽  
Phospholipase A2 ◽  
Physiological Role ◽  
Peritoneal Macrophages ◽  
Triggered Release ◽  
Patch Clamp Technique ◽  
Cytoplasmic Phospholipase A2 ◽  
Induced Changes ◽  
Stimulation Of

The potential role of cytosolic phospholipase A2 (cPLA2) in the regulation of the electrogenic arachidonic acid (AA)-activatable H+ translocator of neutrophils was investigated. (1) The trifluoromethyl ketone analogue of arachidonate (AACOCF3), a newly developed selective blocker of cPLA2, inhibited both the N-formylmethionyl-leucylphenylalanine (fMLP)- and the phorbol-ester-induced rheogenic H+ efflux (K0.5 ≈ 5 μM) and abrogated the stimulus-triggered release of AA from these cells. The drug failed to reduce the fMLP-evoked Ca2+ signal or protein tyrosine phosphorylation and did not affect the activity of protein kinase C. By using the patch-clamp technique we verified that the agent did not interfere with the voltage- and the pH-dependent activation of the H+ conductance of the peritoneal macrophages and therefore is not a direct blocker of the H+ channel itself. AACOCF3, however, slightly decreased the AA-induced stimulation of the H+ currents. We conclude that AA, liberated by the agonist-induced stimulation of cPLA2, is a direct activator of H+ conductance. (2) AACOCF3 did not inhibit superoxide generation, indicating that activation of cPLA2 may not be a prerequisite for turning on NADPH oxidase. (3) Since neither acid generation by the oxidase, nor the basal or stimulated Na+/H+ exchange (the predominant acid-eliminating mechanism) were influenced by the drug, we could use AACOCF3 to address whether the H+ channel in fact opens and plays any physiological role during activation of neutrophils. Stimulus-induced cytosolic alkalinization was smaller, whereas depolarization became larger, in the presence of AACOCF3. Stimulated H+ conductance therefore does contribute to intracellular pH (pHi) homoeostasis and membrane potential changes of intact neutrophils.

Ca2+-dependent p47phox translocation in hydroperoxide modulation of the alveolar macrophage respiratory burst

1997 ◽  
Vol 273 (5) ◽  
pp. L1042-L1047 ◽  
Author(s):  
Huanfang Zhou ◽  
Roger F. Duncan ◽  
Timothy W. Robison ◽  
Lin Gao ◽  
Henry Jay Forman
Keyword(s):  
Oxidative Stress ◽  
Plasma Membrane ◽  
Alveolar Macrophages ◽  
Respiratory Burst ◽  
Tert Butyl Hydroperoxide ◽  
Intracellular Ca ◽  
Induced Changes ◽  
Respiratory Burst Oxidase ◽  
Dependent Processes ◽  
Stimulation Of

Oxidative stress produces dual effects on the respiratory burst of rat alveolar macrophages. Preincubation with hydroperoxide concentrations [H2O2or tert-butyl hydroperoxide ( t-BOOH); <50 μM] enhances stimulation of the respiratory burst, whereas higher concentrations inhibit stimulation. Both the enhancement and inhibition are markedly attenuated by buffering t-BOOH-induced changes in intracellular Ca2+concentration ([Ca2+]i). Phosphorylation of the NADPH oxidase component p47phox and its translocation from cytoplasm to plasma membrane are essential in respiratory burst activation. Phorbol 12-myristate 13-acetate (PMA)-stimulated p47phox phosphorylation was negligibly affected by 25 or 100 μM t-BOOH. Nonetheless, 25 μM t-BOOH increased PMA-stimulated p47phox translocation, whereas 100 μM t-BOOH decreased PMA-stimulated translocation. In unstimulated cells, however, neither phosphorylation nor translocation of p47phox was affected by t-BOOH. Buffering of the t-BOOH-mediated changes of [Ca2+]iabolished the effects of t-BOOH on PMA-stimulated translocation in parallel to effects upon the respiratory burst. The results suggest that the dual effects of hydroperoxides are mediated, in part, by Ca2+-dependent processes affecting the assembly of the respiratory burst oxidase at steps that are separate from p47phoxphosphorylation.

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