Contribution of an electrogenic sodium pump to the membrane potential in rabbit sinoatrial node cells

1975 ◽  
Vol 358 (4) ◽  
pp. 289-301 ◽  
Author(s):  
Akinori Noma ◽  
Hiroshi Irisawa
2001 ◽  
Vol 537 (2) ◽  
pp. 467-488 ◽  
Author(s):  
Kageyoshi Ono ◽  
Haruko Masumiya ◽  
Aiji Sakamoto ◽  
Georges Christé ◽  
Toshinori Shijuku ◽  
...  

1978 ◽  
pp. 301-310 ◽  
Author(s):  
Akinori Noma ◽  
Kaoru Yanagihara ◽  
Hiroshi Irisawa

1995 ◽  
Vol 269 (2) ◽  
pp. H443-H452 ◽  
Author(s):  
H. Ito ◽  
K. Ono

The single-channel current of the delayed rectifier K+ current (IK) was recorded in rabbit sinoatrial node cells. In the cell-attached patch, depolarization from -70 mV to potentials more positive than -50 mV activated the IK channel while repolarization deactivated it. The single-channel conductance was 7.8 pS for the outward current and 10.8 pS for the inward current (n = 6). The steady-state open probability (NPo) was maximum at around -30 mV and markedly decreased at more positive potentials. On repolarization from positive potentials, the channel was initially closed and then rapidly opened. The ensemble average showed an initial rise to a peak followed by the deactivation time course. Because the channel events were completely blocked by E-4031, the drug-sensitive component was examined in the whole cell current. The steady-state current-voltage relation of the drug-sensitive current showed a marked negative slope at potentials more positive than -10 mV. Upon repolarization, the drug-sensitive current initially increased (removal of inactivation) to the peak of the outward tail current, which was in agreement with the ensemble average of the single-channel current. We conclude that IK in the sinoatrial node cells is largely composed of the rapidly activating IK (IK,r) channels and that the inward rectification of IK,r, which is more marked than had been assumed in previous studies, is due to the decrease in NPo.


1978 ◽  
Vol 56 (6) ◽  
pp. 545-551 ◽  
Author(s):  
Stephen Benderoff ◽  
Rose M. Johnstone ◽  
Rhoda Blostein

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.


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