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Potassium channels resting membrane potential

The resting membrane potential of most excitable cells is around —60 to —80 mV. This gradient is maintained by the activity of various ion channels. When the potassium channels of the cell open, potassium efflux occurs and hyperpolari2ation results. This decreases calcium channel openings, which ia turn preveats the influx of calcium iato the cell lea ding to a decrease ia iatraceUular calcium ia the smooth muscles of the vasculature. The vascular smooth muscles thea relax and the systemic blood pressure faUs. [Pg.143]

The ventricular action potential is depicted in Fig. 6-2.2 Myocyte resting membrane potential is usually -70 to -90 mV, due to the action of the sodium-potassium adenosine triphosphatase (ATPase) pump, which maintains relatively high extracellular sodium concentrations and relatively low extracellular potassium concentrations. During each action potential cycle, the potential of the membrane increases to a threshold potential, usually -60 to -80 mV. When the membrane potential reaches this threshold, the fast sodium channels open, allowing sodium ions to rapidly enter the cell. This rapid influx of positive ions... [Pg.109]

In normal atrial and ventricular myocytes, phase 4 is electrically stable, with the resting membrane potential held at approximately -90 mV and maintained by the outward potassium leak current and ion exchangers previously described. It is during phase 4 that the Na+ channels necessary for atrial and ventricular myocyte depolarization recover completely from inactivation. In myocytes capable of automaticity, the membrane potential slowly depolarizes during this period to initiate an action potential (discussed later). [Pg.163]

The state of the sodium channel varies in healthy ventricular cells and those damaged by ischemia. This variability in the state has implications for antiarrhymic therapy with sodium channel blocking agents. In sick or damaged ventricular cells (i.e., from ischemia or blockade of the sodium/potassium-ATPase [sodium/potassium pump]), the resting membrane is more positive than the healthy resting membrane potential (Figure 12.10). [Pg.257]

Keywords Action potential Calcium Glia Ion channel LTP Neuron Neurotransmitter Potassium Resting membrane potential Sodium Structure Synapse... [Pg.107]

Figure 6. Resting membrane potential under normoxia (left) and ischemia (right). Increased outward potassium current during ischemia causes shortening of the resting membrane potential. Potassium currents activated under physiological conditions are inhibited under ischemia and several other new channels come to the operation (IKATp, IKFFA). Resting membrane potential is less negative due to the increased extracellular potassium and inward currents. Figure 6. Resting membrane potential under normoxia (left) and ischemia (right). Increased outward potassium current during ischemia causes shortening of the resting membrane potential. Potassium currents activated under physiological conditions are inhibited under ischemia and several other new channels come to the operation (IKATp, IKFFA). Resting membrane potential is less negative due to the increased extracellular potassium and inward currents.
The assays are based on membrane potential sensitive fluorescent dyes, which are relocated from the inside of the cells (or vice versa) and cause an alteration in the fluorescence intensity or flip between the inner and the outer sides of the membrane bilayer and transfer fluorescence resonance energy to another dye located outside of the membrane [25, 26]. In this assay, cells, transfected with hERG potassium channel, contribute to the resting membrane potential and the inhibition of this channel by test compounds results in depolarization of the cell membrane, entry of fluorescent dye in... [Pg.54]

Quantitatively, the usual resting membrane potential of — 70 mV Is close to but lower In magnitude than that of the potassium equilibrium potential calculated from the Nernst equation because of the presence of a few open Na channels. These open Na channels allow the net Inward flow of Na" ions, making the cytosolic face of the plasma membrane more positive, that is, less negative, than predicted by the... [Pg.262]

Na" ", K", and d are the most important ions for determining membrane potential in human cells. The importance of each ion in determining the resting membrane potential depends on the permeability of each ion in the membrane permeability depends on the number of non-gated channels available for that ion. For many mammalian cells, the net membrane potential is -60 mV, which is closer to the equilibrium potential of potassium than sodium due to the greater permeability of resting membranes to potassium. [Pg.134]

Birinyi-Strachan et al. used patch-clamp recording techniques on rat dorsal root ganglion neurons in order to study the blockage of voltage-gated potassium channels by CTX-1, specifically delayed-rectifier potassium (Kqr) channels and transient A-type potassium (Ka) channels. They observed that in addition to cause a depolarization of the resting membrane potential and a significant increase... [Pg.616]

Pumiliotoxin B had no apparent effect on sodium, potassium or chloride conductances or on resting membrane potential 24). The potentiative effects of pumiliotoxin B were fully manifest in preparations in which acetylcholine receptors were blocked by a-bungarotoxin. Dantrolene, an agent which appears to interfere with release of calcium from the sarcoplasmic reticulum and methoxyverapamil, a purported antagonist of calcium channels, only partially prevented the effects of pumiliotoxin B on muscle contractions. [Pg.313]

In a resting condition, there is a specific rest potential between the axoplasm and the inner parts of the cell. This rest potential is maintained by relative concentration of sodium and potassium ions along the membrane of the nerve. During nerve stimulation, the membrane is depolarized and sodium channels in that area are opened, allowing sodium ions to rush into the cell. At the peak of depolarization potassium channels are opened. The last ones leave the cell and the cell is repolarized. [Pg.10]


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