Anoxia decreases the transient K+ outward current in isolated ventricular heart cells of the mouse

1994 ◽  
Vol 427 (5-6) ◽  
pp. 547-549 ◽  
Author(s):  
S. Thierfelder ◽  
H. Hirche ◽  
K. Benndorf
Keyword(s):  
Outward Current ◽  
Heart Cells ◽  
K Outward Current

Ca-Induced K+-Outward Current in Paramecium Tetraurelia

1980 ◽  
Vol 88 (1) ◽  
pp. 293-304 ◽  
Author(s):  
YOUKO SATOW ◽  
CHING KUNG
Keyword(s):  
Steady State ◽  
Voltage Clamp ◽  
Outward Current ◽  
Paramecium Tetraurelia ◽  
Ca Channels ◽  
Outward Currents ◽  
Ciliary Reversal ◽  
Voltage Dependent ◽  
K Current ◽  
K Outward Current

Late K-outward currents upon membrane depolarization were recorded in Paramecium tetraurelia under a voltage clamp. A Ca-induced K-outward component is demonstrated by subtracting the value of the outward current in a pawn A mutant lacking functional Ca-channels (pwA500). The Ca-induced K-outward current activates slowly, reaching a peak after 100 to 1000 ms. The current then remains steady or reaches the steady state after a decline of several seconds. EGTA2- injection experiments show that the Ca-induced K-outward current is dependent on the internal Ca2+ concentration. The current is shown to depend on the voltage-dependent Ca conductance, by study of the leaky pawn A mutant (pwA132), which has a lowered Ca conductance as well as a lowered Ca-induced K-current. The Ca-induced GK is thus indirectly dependent on the voltage. The maximal GK is about 40 nmho/cell at + 7 mV in 4 mM-K+. The Ca-induced K current is sustained throughout the prolonged depolarization and the prolonged ciliary reversal.

Sensitivity of Cardiac Background Inward Rectifying K+Outward Current (IK1) to the Alkaloids Lepadiformines A, B, and C

2006 ◽  
Vol 69 (4) ◽  
pp. 558-562 ◽  
Author(s):  
Martin-Pierre Sauviat ◽  
Joseph Vercauteren ◽  
Nicole Grimaud ◽  
Marcel Jugé ◽  
Mohamed Nabil ◽  
...  
Keyword(s):  
Outward Current ◽  
K Outward Current

scholarly journals Changes in external Na induce a membrane current related to the Na-Ca exchange in cesium-loaded frog heart cells.

1984 ◽  
Vol 84 (2) ◽  
pp. 201-220 ◽  
Author(s):  
D Mentrard ◽  
G Vassort ◽  
R Fischmeister
Keyword(s):  
Membrane Potential ◽  
Outward Current ◽  
Current Amplitude ◽  
Frog Heart ◽  
Heart Cells ◽  
Ca Ions ◽  
Standard Solution ◽  
A Current ◽  
K Currents ◽  
Intact Heart

The effects of transient alterations in Nao were investigated under voltage clamp conditions in frog heart cells previously loaded with Cs. Tetrodotoxin and Cs were used to inhibit Na and K currents. On applying a Na-poor solution (39.2 mM), an outward current was generated during both depolarizations and hyperpolarizations. The current amplitude described a U-shaped function of the membrane potential. On reapplying the standard solution after 15 min equilibration, an inward current was then induced that exhibited a bell-shaped function of the membrane potential. Current amplitude was sensitive to the external Ca concentration. Increasing pHi by 10 mM NH4Cl enhanced this current, while the internal acidification that occurred on switching back to the control solution greatly reduced it. Variations in the amplitude of this current during repetitive stimulations or long pauses are best explained by subsequent alterations in Nai and pHi; no evidence for a time dependence was found. This current was inhibited by La3+, Co2+, and D600, and was sensitive to adriamycin, quinidine, and disopyramide; lidocaine, another local anesthetic, and nifedipine had no effect. These observations extend previous work on intact heart cells and sarcolemmal vesicles. They suggest that the Na-Ca exchange may generate a current that is outward when Ca ions are moving into the cell.

scholarly journals KV2.1 K+ Channels Underlie Major Voltage-Gated K+ Outward Current in H9c2 Myoblasts.

2002 ◽  
Vol 52 (6) ◽  
pp. 507-514 ◽  
Author(s):  
Wei Wang ◽  
Naoki Hino ◽  
Hiroshi Yamasaki ◽  
Takashi Aoki ◽  
Rikuo Ochi
Keyword(s):  
Outward Current ◽  
K Channels ◽  
Voltage Gated ◽  
H9c2 Myoblasts ◽  
K Outward Current

Inflammatory stimuli induce a new K+ outward current in cultured rat microglia

1992 ◽  
Vol 147 (2) ◽  
pp. 171-174 ◽  
Author(s):  
Wolfgang Nörenberg ◽  
Peter J. Gebicke-Haerter ◽  
Peter Illes
Keyword(s):  
Outward Current ◽  
Inflammatory Stimuli ◽  
K Outward Current

Slowly inactivating outward currents in a cuticular mechanoreceptor neuron of the cockroach (Periplaneta americana)

1995 ◽  
Vol 74 (3) ◽  
pp. 1200-1211 ◽  
Author(s):  
P. H. Torkkeli ◽  
A. S. French
Keyword(s):  
Voltage Clamp ◽  
Time Constant ◽  
Action Potentials ◽  
Periplaneta Americana ◽  
Outward Current ◽  
Equilibrium Potential ◽  
Channel Blockers ◽  
Outward Currents ◽  
Frequency Of Action Potentials ◽  
K Outward Current

1. Although rapid adaptation is a widespread feature of sensory receptors, its ionic basis has not been clearly established in any touch receptor, because their small sizes have severely restricted the range of experiments tat can be performed. In the cockroach tactile spine, intracellular voltage-clamp recordings are now possible. 2. The basic electrophysiological properties of the cockroach femoral tactile spine neuron were studied using discontinuous (switching) single-electrode current- and voltage-clamp recordings. A slowly inactivating voltage-sensitive K+ outward current was detected after the major inward currents were blocked with tetrodotoxin. 3. The total outward current activated in < 1 ms at voltages above 0 mV. At moderate depolarizations it did not inactivate, but at higher depolarizations an inactivation time constant of approximately 260 ms was measured. Some recordings also revealed an additional, slower inactivation time constant of approximately 2.5 s. 4. More than half of the voltage-sensitive K+ outward current could be blocked with the Ca2+ channel blockers Co2+ and Cd2+. Tetraethylammonium chloride (TEA) also reduced the amplitude of the outward current to about half of its original amplitude. The actions of both blockers were reversible and probably reflect overlapping blockades of two separate outward currents. 5. The reversal potentials of the currents that remained after block with Co2+ (-91.7 mV) or TEA (-86.8 mV) were both near the K+ equilibrium potential expected for the tactile spine neuron. The voltage dependencies of activation of the Co(2+)- and TEA-resistant currents were both well fitted by Boltzmann distributions, giving values of half maximal activation (V50) equal to -34.5 mV for the Co(2+)-resistant current and -51.3 mV for the TEA-resistant current. 6. Current-clamp recordings revealed that the TEA-sensitive K+ current was the major component of action potential repolarization but that it did not effect the frequency of action potentials evoked by steady depolarization. On the other hand, blockers of Ca(2+)-sensitive K+ currents (Cd2+, Co2+, or charybdotoxin) reduced adaptation and increased the frequency of action potentials significantly but did not effect the duration or amplitude of individual action potentials.

scholarly journals Voltage clamp analysis of embryonic heart cell aggregates.

1979 ◽  
Vol 73 (2) ◽  
pp. 175-198 ◽  
Author(s):  
R D Nathan ◽  
R L DeHaan
Keyword(s):  
Voltage Clamp ◽  
Voltage Dependence ◽  
Slow Component ◽  
Outward Current ◽  
Heart Cell ◽  
Heart Cells ◽  
Spatial Homogeneity ◽  
Inward Current ◽  
Maximal Activation ◽  
Inward Currents

The double-microelectrode voltage clamp technique was applied to small spheroidal aggregates of heart cells from 7-d chick embryos. A third intracellular electrode was sometimes used to monitor spatial homogeneity. On average, aggregates were found to deviate from isopotentiality by 12% during the first 3--5 ms of large depolarizing voltage steps, when inward current was maximal, and by less than 3% thereafter. Two components of inward current were recorded: (a) a fast, transient current associated with the rapid upstroke of the action potential, which was abolished by tetrodotoxin (TTX); and (b) a slower inward current related to the plateau, which was not affected by TTX but was blocked by D600. The magnitudes, kinetics, and voltage dependence of these two inward currents and a delayed outward current were similar to those reported for adult cardiac preparations. From a holding potential of -60 mV, the peak fast component at the point of maximal activation (-20 mV) was -185 microA/cm2. This value was about seven times greater than the maximal slow component which peaked at 0 mV. The ratio of rate constants for the decay of the two currents was between 10:1 and 30:1.

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