Potassium equilibrium potential

The excitable membrane of nerve axons, like the membrane of cardiac muscle (see Chapter 14) and neuronal cell bodies (see Chapter 21), maintains a resting transmembrane potential of -90 to -60 mV. During excitation, the sodium channels open, and a fast inward sodium current quickly depolarizes the membrane toward the sodium equilibrium potential (+40 mV). As a result of this depolarization process, the sodium channels close (inactivate) and potassium channels open. The outward flow of potassium repolarizes the membrane toward the potassium equilibrium potential (about -95 mV) repolarization returns the sodium channels to the rested state with a characteristic recovery time that determines the refractory period. The transmembrane ionic gradients are maintained by the sodium pump. These ionic fluxes are similar to, but simpler than, those in heart muscle, and local anesthetics have similar effects in both tissues. 

Final repolarization (phase 3) of the action potential results from completion of sodium and calcium channel inactivation and the growth of potassium permeability, so that the membrane potential once again approaches the potassium equilibrium potential. The major potassium currents involved in phase 3 repolarization include a rapidly activating potassium current (Ikt) and a slowly activating potassium current (Iks)- These processes are diagrammed in Figure 14-3. 

The resting membrane potential of the muscle and nerve is known to be close to the Cl" equilibrium potential. The potassium equilibrium potential is also close to the resting membrane potential. When the muscles are exposed to the K+ free solution, the resting membrane potential is known to hyperpolarize below the chloride ion equilibrium potential (28). When the avermectin-treated muscles were exposed to the K free saline solution containing 3 C1, the 3 C1 influx was suppressed to 60% of the control. 

If the membrane is permeable only to ions and not to Na or CP ions, then a similar equation describes the potassium equilibrium potential k ... 

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... 

The first section of Table II represents the transepithelial parameters. The fluid/plasma K activity ratio of 1.9 0.2 is significantly greater than unity (P < 0.01) but is not significantly different from an inulin ratio of 1.5 0.2 in the latter part of the proximal tubule of the Necturus kidney. The potassium equilibrium potential (Ej ) calculated from the Nernst equation using the K" " activity ratio yield a value of 16.4 1.0 mV. This is not significantly different from the mean transepithelial PD of 14.5 A 1.5 mV. Thus K ion is in electro-chemical equilibrium distribution across the proximal tubular epithelium of Necturus. 

It should be noted, however, that if you are only interested in the difference between % and Er (the potassium equilibrium potential), that number can be obtained from AE alone. Using the definition of Er, equation 1 can be written in the form shown as equation 2 in which the last term on the right side is known ... 

Oyama Y, Walker JL, Eyzaguirre C. Intracellular potassium activity, potassium equilibrium potential and membrane potential of carotid body glomus cells. Brain Res 1986 381 405 08. 

Three kinds of equilibrium potentials are distinguishable. A metal-ion potential exists if a metal and its ions are present in balanced phases, e.g., zinc and zinc ions at the anode of the Daniell element. A redox potential can be found if both phases exchange electrons and the electron exchange is in equilibrium for example, the normal hydrogen half-cell with an electron transfer between hydrogen and protons at the platinum electrode. In the case where a couple of different ions are present, of which only one can cross the phase boundary — a situation which may exist at a semiperme-able membrane — one obtains a so called membrane potential. Well-known examples are the sodium/potassium ion pumps in human cells. 

Table 3. Comparison of experimental and calculated equilibrium potentials for various gas environments and electrolyte compositions, 400 °C, relative to Ag/Ag+ reference. Results are reported on the basis of changes in the equilibrium potential relative to a base case of pure potassium pyrosulfate under an air environment.

Thus, the contribution of each ion to the overall membrane potential depends not only on its concentration but it is weighted for the permeability of the membrane for that ion. Since the concentrations and gradients for and Na are of similar magnitude, we may infer that the membrane permeability must be larger for potassium than for sodium (Pk > P g), since the actual membrane potential is much closer to the than to the Na equilibrium potential. 

The opening of the voltage-gated potassium channels, which will pull the membrane potential back into the direction of the equilibrium potential. 

Simply put, the action potential is caused by a state of disequilibrium between ideal electrical potentials for two ions, sodium and potassium. The equilibrium potentials for Na" " and K can be thought of as the electrical force required to maintain the given ionic gradients across the cell membrane for each ion. For Na" ", the equilibrium potential is approximately 50 mV (with respect to the inside of the membrane) for K +, it is approximately —75 mV. (These values apply to the giant squid axon on which the early investigations on action potentials were conducted. Of course, these values... 

Glycosides increase intracellular sodium and also extracellular potassium by inhibitory actions on sodium potassium ATPase. Thus, with chronic therapy, because intracellular sodium is increased, phase 0 may be blunted slightly. The increase in extracellular potassium results in a decrease in the rate of repolarization and thus a decrease in the slope of phase 3 of the action potential, and a skewed appearance. This results in a longer time for the membrane to repolarize and, accordingly, an increase in the effective refractory period. Because the objective of the drug is to increase the influx of calcium, the faster influx of calcium results in a shortened phase 2, because a shorter time is required for the membrane to reach the equilibrium potential for calcium. Finally, phase 4 is elevated and increased in slope, due to the alterations in sodium and potassium concentration. This, with chronic therapy, and particularly as toxicity is approached, results in delayed oscillatory afterpotentials (see Figure). 

The major determinants of cardiac action are sodium, potassium, and calcium. The equilibrium potentials are sodium = +60, potassium = -90, calcium = +50... 

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. 

Formerly, the membrane potential in biological cells was thought to be due to this Donnan equilibrium potential. Bernstein suggested that the resting membrane potential was determined by the ratio of potassium ion concentration inside and outside the cell. The relative impermeability of Na" across the cell membrane was observed by Boyle and Conway. The validity of the formula of the membrane potential for biological cells... 

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