Electrogenic sodium-dependent glycine transport in sheep reticulocytes

1978 ◽  
Vol 56 (6) ◽  
pp. 545-551 ◽  
Author(s):  
Stephen Benderoff ◽  
Rose M. Johnstone ◽  
Rhoda Blostein
Keyword(s):  
Membrane Potential ◽  
Sodium Pump ◽  
Marked Decrease ◽  
Massive Bleeding ◽  
Atp Content ◽  
Chemical Gradient ◽  
Electrogenic Sodium Pump ◽  
Sodium Dependent ◽  
Glycine Transport ◽  
Measurable Change

Na+-dependent glycine transport has been studied in reticulocyte-enriched fractions of blood obtained after massive bleeding of sheep. The activity is dependent on the sodium electrochemical potential and the membrane potential. The sodium chemical gradient was varied by changing either external or internal Na+ and the membrane potential, by addition of valinomycin. Similar results were obtained with resealed reticulocyte ghosts. Under conditions optimal for sodium pumping (intracellular Na+ > 50 mM), ouabain inhibited glycine uptake prior to any measurable change in the cellular Na+ suggesting that in these cells an electrogenic sodium pump is sufficiently active to contribute to the membrane potential. Na+-dependent glycine transport undergoes a marked decrease during Song-term incubation at 37 °C. During this time, the cells maintain their integrity and ATP content but undergo maturation as evidenced in the decrease in cells with reticulocyte morphology.

scholarly journals Sodium and potassium fluxes and membrane potential of human neutrophils: evidence for an electrogenic sodium pump.

1982 ◽  
Vol 79 (3) ◽  
pp. 453-479 ◽  
Author(s):  
L Simchowitz ◽  
I Spilberg ◽  
P De Weer
Keyword(s):  
Membrane Potential ◽  
Sodium Pump ◽  
Membrane Conductance ◽  
Human Neutrophils ◽  
Constant Field ◽  
Electrogenic Sodium Pump ◽  
Na Efflux ◽  
The Individual ◽  
Sodium And Potassium ◽  
External K

Sodium and potassium ion contents and fluxes of isolated resting human peripheral polymorphonuclear leukocytes were measured. In cells kept at 37 degrees C, [Na]i was 25 mM and [K]i was 120 mM; both ions were completely exchangeable with extracellular isotopes. One-way Na and K fluxes, measured with 22Na and 42K, were all approximately 0.9 meq/liter cell water . min. Ouabain had no effect on Na influx or K efflux, but inhibited 95 +/- 7% of Na efflux and 63% of K influx. Cells kept at 0 degree C gained sodium in exchange for potassium ([Na]i nearly tripled in 3 h); upon rewarming, ouabain-sensitive K influx into such cells was strongly enhanced. External K stimulated Na efflux (Km approximately 1.5 mM in 140-mM Na medium). The PNa/PK permeability ratio, estimated from ouabain insensitive fluxes, was 0.10. Valinomycin (1 microM) approximately doubled PK. Membrane potential (Vm) was estimated using the potentiometric indicator diS-C3(5); calibration was based on the assumption of constant-field behavior. External K, but not Cl, affected Vm. Ouabain caused a depolarization whose magnitude dependent on [Na]i. Sodium-depleted cells became hyperpolarized when exposed to the neutral exchange carrier monensin; this hyperpolarization was abolished by ouabain. We conclude that the sodium pump of human peripheral neutrophils is electrogenic, and that the size of the pump-induced hyperpolarization is consistent with the membrane conductance (3.7-4.0 microseconds/cm2) computed from the individual K and Na conductances.

Action of acetylcholine on the longitudinal muscle of guinea-pig ileum: the role of an electrogenic sodium pump

1973 ◽  
Vol 265 (867) ◽  
pp. 107-114 ◽  
Keyword(s):  
Membrane Potential ◽  
Guinea Pig ◽  
Sodium Pump ◽  
Longitudinal Muscle ◽  
Membrane Resistance ◽  
Free Solution ◽  
Electrogenic Sodium Pump ◽  
External Potassium ◽  
Sodium And Potassium

Intracellular recordings of membrane potential were made from the longitudinal muscle of guinea-pig terminal ileum. It was observed that ouabain or potassium-free solution depolarized the membrane. Upon readmitting potassium to potassium-free solution, the membrane potential rapidly increased. This response was blocked by ouabain and was potentiated in chloride-deficient solution, suggesting that it was due to the activity of an electrogenic sodium pump. When acetylcholine was applied, and then washed from the tissue, there followed a period of increased negativity of the membrane potential, an after-hyperpolarization. This did not occur when responses to acetylcholine were obtained in the presence of ouabain, in potassium-free solution, or in sodium-deficient solution, but the after-hyperpolarization was increased in size in chloride-deficient solution. During a 2 min application of carbachol, the membrane potential fell more rapidly in the presence of ouabain (10 -5 mol/1); this could be explained if sodium pump activity is important in retarding the decline of the sodium and potassium gradients that occurs at this time. It was concluded that the application of acetylcholine or carbachol to ileal muscle increases internal sodium and probably external potassium concentrations. These increases stimulate the activity of the electrogenic sodium pump so that, when the membrane resistance recovers, there is an increased electrogenic contribution to the membrane potential. This produces the after-hyperpolarization which is a feature of the response to acetylcholine.

Type 1 Sodium-Dependent Phosphate Transporter acts as a Membrane Potential-Driven Urate Exporter

2013 ◽  
Vol 6 (2) ◽  
pp. 88-94 ◽  
Author(s):  
Takaaki Miyaji ◽  
Tatsuya Kawasaki ◽  
Natsuko Togawa ◽  
Hiroshi Omote ◽  
Yoshinori Moriyama
Keyword(s):  
Membrane Potential ◽  
Phosphate Transporter ◽  
Sodium Dependent
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