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What effect does potassium have on the resting potential of a cardiac cell?
Wiki User
∙ 11y ago
Hyperkalemia is an increase in extracellular K. Driving force of an ion depends on two factors, voltage and concentration gradient. For K voltage gradient is pushing K into the cell but the concentration gradient is driving K out of the cell. However, the total driving force for K is out of the cell because the concentration gradient is that strong. When there is an increase in K on the outside, the driving force for K decreases.
The equilibrium potential for K is -95mV. This means if K was freely permeable to the cell's membrane, it would reach equilibrium at -95mV. Another way to look at this is that efflux of K is the same as influx of K and the cell's new resting membrane potential would increase from a normal value of -70mV to -95mV. Note that I said it would increase even though the value became more negative. This is because the change in membrane potential has increased.
Since the driving force of K has decreased, the equilibrium potential has also decreased. From a value of -95mV it is decreased to let's just say -80mV. Since a normal resting membrane potential is regularly -70mV, the decrease in equilibrium potential of K has decreased this resting membrane potential to say -60mV now. This is a depolarization of the cell.
If this process happens quickly, it will depolarize the cell to the threshold value and you will have an action potential. However, if the hyperkalemia is severe, the cell will stay depolarized because the K equilibrium has decreased to a point where the cell cannot hyperpolarize back to threshold or resting membrane potential.
If this process happens slowly, the inactivation gates of the sodium voltage-gated channels will automatically shut and the cell cannot depolarize even if it reaches threshold values. It must hyperpolarize back to resting membrane potential and the inactivation gates of the sodium voltage-gated channel will reopen.
Wiki User
∙ 13y ago
Wiki User
∙ 11y agoIn the case of potassium, its diffusion down its concentration gradient, toward the outside of the cell, creates transmembrane voltage potential. Blocking these channels will not allow the concentration gradient to create a voltage at all. Ultimately producing a resting membrane potential of zero
Wiki User
∙ 13y agoHyperkalemia decreases the membrane potential which will result in a depolarization.
Wiki User
∙ 11y agoIncreasing extracellular potassium causes the resting membrane potential to become more positive.
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What would happen to a resting membrane potential if the sodium potassium transport pump was blocked?
During depolarization, sodium (Na) rushes into the neuron through Na channels (at the Nodes of Ranvier between the bundles of myelin "insulation"). Less Na in the extracellular fluid would mean there would be less to rush in. So, the neuron would not be depolarized as well. The resting membrane potential would be more positive on the inside.
What effect will Raising the potassium ion concentration in the extracellular fluid surrounding a nerve cell have?
Both hyperpolarize it and decrease the magnitude of the potassium equilibrium potential.
What effect would the presence of potassium hydroxide have on starch production?
Potassium hydroxide removes carbon. It also helps to break down starch. Therefore, potassium hydroxide would mean less starch production.
What would be the effect on action potential conduction at a region of axon where the disease had its effect?
Depends on disease
What the Effect of ouabain drug on a neuron ability to generate action potential?
what effect does the drug quabain have on neuron
What effect does hypocalcemia have on the cardiac action potential?
It can prolong the cardiac action potential. It can also have other effects, such as torsades de pointes,and it can mask digitalis toxicity.
What would happen to a resting membrane potential if the sodium potassium transport pump was blocked?
During depolarization, sodium (Na) rushes into the neuron through Na channels (at the Nodes of Ranvier between the bundles of myelin "insulation"). Less Na in the extracellular fluid would mean there would be less to rush in. So, the neuron would not be depolarized as well. The resting membrane potential would be more positive on the inside.
Which electrolyte helps regulate cardiac impulse transmission and muscle contraction?
Potassium has the main direct effect on cardiac impulse transmission and muscle contraction. However, potassium (K+) and sodium (Na) have an inverse relationship; when one is increased the olther is decreased. In cardiac health, both must be balanced to effect homeostasis. This is why repeat electrolyte lab values and cardiac enzymes are so important in unstable cardiac patients.
Major determinant of the resting potential of all cells is?
Resting membrane potential is determined by K+ concentration gradient and cell's resting permeability to K+, N+, and Cl-.Gated channels control ion permeability. Three types of gated channels are mechanically gated, chemical gated, voltage gated. Threshold voltage varies from one channel type to another.The Goldmann- Hodgkins-Katz Equation predicts membrane potential using multiple ionsThe resting potentialBecause the plasma membrane is highly permeable to potassium ions, the resting potential is fairly close to -90mV, the equilibrium potential for K+Although the electrochemical gradient for sodium ions is very large, the membrane's permeability to these ions is very low. Consequently, Na+ has only a small effect on the normal resting potential, making it just slightly less negative than it would be otherwise.The sodium-potassium exchange pump ejects 3 Na+ ions for every 2 K+ ions that it brings into the cell. It thus serves to stabilize the resting potential when the ratio of Na+ entry to K+ loss through passive channels is 3:2.At the normal resting potential, these passive and active mechanisms are in balance. The resting potential varies widely with the type of cell. A typical neuron has a resting potential of approx -70mV
What effect will Raising the potassium ion concentration in the extracellular fluid surrounding a nerve cell have?
Both hyperpolarize it and decrease the magnitude of the potassium equilibrium potential.
What was the effect of ether on elicciting an action potential?
Ether causes potassium ion pores to open, allowing potassium ions to leave the neuron, hyper-polarizing the neuron so it is unable to fire an action potential.
What effect does the leaking of potassium across the membrane have on the membrane potential of Kevin's neurons?
It makes the inside of the neurons more negative.
What is the effect of lidocaine on eliciting an action potential?
Ether prevents the action potential, by opening potassium ion pores, which allows the escape of potassium from the neurons, which results in hyper-polarization of the neuron, thus preventing the action potential from occurring.
Where does the sodium potassium release potassium ions?
The "fast" voltage-gated sodium channels open at -55 mV and close at about +60 mV. I found your question by attempting to find an answer to its second part which is "when [do]...potassium channels open..." and I have yet to find the answer to this myself! There are lots of graphs in physiology books which indicate it is at a voltage very close to that of the sodium channel but I have yet to find an actual figure! The important thing to know is that the potassium channels open at a similar time but are much slower at allowing potassium to flow out of the cell. The effect is that the influx of sodium rapidly brings the resting membrane potential from it's threshold potential of -55 mV to its peak of about +60 mV, at which point they close and become refractory. The slower potassium efflux then "catches up" and brings the membrane potential back down towards its resting value and actually causes a small over-shoot known as hyperpolarisation. The net change in cytosol concentration of the ions is minimal and quickly reversed by the magnificent Sodium-Potassium-ATPase. If you come across the answer to the opening voltage of the potassium channels, please let me know!
What would be the most immediate effect of doubling the number of Na leakage channels in the plasma membrane?
The resting membrane potential would become less negative (more positive).
What has the author Bert A Mobley written?
Bert A. Mobley has written: 'The effect of potassium and chloride ions on the volume and membrane potential of single barnacle muscle cells'
What happens in each of the five phases of cardiac muscle depolarization?
PHASE0(RAPID DEPOLARIZATION) due to opening of fast voltage gated sodium channels PHASE1(INITIAL REPOLARIZATION) due to closure of sodium channels while loss of potassium is goingon ,making the cell polarized. PHASE2(PLATEAU) due to opening of calcium channels. influx of calcium neutralizes the effect of out going potassium so prolonged plateau is achieved. PHASE3(FINAL RE POLARIZATION) due to closure of calcium channels and continue loss of potassium makes the inside of cell more negative resulting in polarization. PHASE4(RMP) eventually cell returns to resting membrane potential due to K efflux and cell is ready for next cycle
