scholarly journals 1P301 Membrane current fluctuations in the modified Oosawa model with Ca-gated K-channels

2004 ◽  
Vol 44 (supplement) ◽  
pp. S104
Author(s):  
N. Hashimoto
Keyword(s):  
Membrane Current ◽  
Current Fluctuations ◽  
K Channels

Voltage-Dependence of Extracellular Ca2+-Induced Modification in Properties of the Inward Rectifying K+ Channels in the Plasma Membrane of Mesophyll Protoplasts of Avena sativa

1996 ◽  
Vol 23 (3) ◽  
pp. 349 ◽  
Author(s):  
J Kourie
Keyword(s):  
Plasma Membrane ◽  
Time Constant ◽  
Avena Sativa ◽  
Voltage Dependence ◽  
Membrane Current ◽  
Time Dependent ◽  
Mesophyll Cells ◽  
K Channels ◽  
Current Passing ◽  
K Current

Data obtained using the whole-celi configuration of the patch-clamp technique reveal that characteristics of the inward rectifying K+ current across the plasma membrane of protoplasts isolated from mesophyll cells of leaves of oat (Avena sativa) are modified by increasing concentrations or removing the extracellular Ca2+. The whole-cell membrane current reveals two components. The first component an initial current II* which is the sum of two currents: (a) a linear ohmic leak current passing through non-gated channels, liNGC, and (b) a rectifying inward K+ current passing through inward rectifying gated K+ channels, IKi, that are instantaneously open. The second component of the membrane current at the steady state Iss is a time-dependent K+ current IKss defined as Iss-IiNGC and passes through inward rectifying gated K+ channels. The tail K+ current, IKT, is also defined as IT-IiNGC. Raising external calcium concentration, [Ca2+]o, from 0.1 mM to 10 mM blocked the inward rectifying currents IKi, IKss and IKT. The voltage-dependence of the activation time constant (τa) for time-dependent KC current IKss was not altered significantly by increasing [Ca2+]o whereas the deactivation time constant (τd) of the IKT increased from 16 ms to 30 ms at a Vm of -100 mV. Removal of [Ca2+]o increased the amplitude and altered the characteristics of the inward rectifying K+ current. Ten minutes after the removal of [Ca2+]o the increase in IKi was 3.5-fold larger than the increase in IKss. Furthermore, removing [Ca2+]o hastened the activation of IKss and the deactivation of IKT. However, the deactivation time constant (Td) remained dependent on membrane voltage (Vm). Extracellular Ca2+ may modulate the function of mesophyll cells by regulating K+ transport through the inward rectifying K+ channels and this may have significant implications for photosynthesis and cell expansion.

scholarly journals Ca2+-activated K+ Channels in Murine Endothelial Cells: Block by Intracellular Calcium and Magnesium

2008 ◽  
Vol 131 (2) ◽  
pp. 125-135 ◽  
Author(s):  
Jonathan Ledoux ◽  
Adrian D. Bonev ◽  
Mark T. Nelson
Keyword(s):  
Endothelial Cells ◽  
Membrane Potential ◽  
Intracellular Calcium ◽  
Membrane Current ◽  
Mesenteric Arteries ◽  
Equilibrium Potential ◽  
Inward Rectification ◽  
Resting Membrane Potential ◽  
Additional Increase ◽  
K Channels

The intermediate (IKCa) and small (SKCa) conductance Ca2+-sensitive K+ channels in endothelial cells (ECs) modulate vascular diameter through regulation of EC membrane potential. However, contribution of IKCa and SKCa channels to membrane current and potential in native endothelial cells remains unclear. In freshly isolated endothelial cells from mouse aorta dialyzed with 3 μM free [Ca2+]i and 1 mM free [Mg2+]i, membrane currents reversed at the potassium equilibrium potential and exhibited an inward rectification at positive membrane potentials. Blockers of large-conductance, Ca2+-sensitive potassium (BKCa) and strong inward rectifier potassium (Kir) channels did not affect the membrane current. However, blockers of IKCa channels, charybdotoxin (ChTX), and of SKCa channels, apamin (Ap), significantly reduced the whole-cell current. Although IKCa and SKCa channels are intrinsically voltage independent, ChTX- and Ap-sensitive currents decreased steeply with membrane potential depolarization. Removal of intracellular Mg2+ significantly increased these currents. Moreover, concomitant reduction of the [Ca2+]i to 1 μM caused an additional increase in ChTX- and Ap-sensitive currents so that the currents exhibited theoretical outward rectification. Block of IKCa and SKCa channels caused a significant endothelial membrane potential depolarization (≈11 mV) and decrease in [Ca2+]i in mesenteric arteries in the absence of an agonist. These results indicate that [Ca2+]i can both activate and block IKCa and SKCa channels in endothelial cells, and that these channels regulate the resting membrane potential and intracellular calcium in native endothelium.

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