The sodium concentration in the red blood cytosol is much lower than the sodium concentration in plasma.

The 2010 Dietary Guidelines for Americans recommend Americans age 2 years and older reduce daily sodium intake to less than 2,300 mg and further reduce intake to 1,500 mg among persons who are 51 and older and those of any age who are African American or have hypertension, diabetes, or chronic kidney disease

1 milli-mole/liter (mmol/L) is 66.459999999998 gram/liter (g/L)

Despite more frequent dialysis, an uncontrolled dietary intakeshould bediscouraged. A daily oral intakeof

 70 g protein, 

1500 mg calcium, 

50 mmol potassium, and 

80 mmol sodium is advised,

Dysfunction in voltage-gated sodium channels correlates with neurological and cardiac diseases, including epilepsy, myopathies, and cardiac arrhythmias

Before an action potential occurs, the axonal membrane is at its normal resting potential, about −70 mV in most human neurons, and Na+ channels are in their deactivated state, blocked on the extracellular side by their activation gates. In response to an increase of the membrane potential to about −55 mV (in this case, caused by an action potential), the activation gates open, allowing positively charged Na+ ions to flow into the neuron through the channels, and causing the voltage across the neuronal membrane to increase to +30 mV in human neurons. Because the voltage across the membrane is initially negative, as its voltage increases to and past zero (from −70 mV at rest to a maximum of +30 mV), it is said to depolarize. This increase in voltage constitutes the rising phase of an action potential.

Action PotentialMembrane PotentialTarget PotentialGate's Target StateNeuron's Target State
Resting−70 mV−55 mVDeactivated → ActivatedPolarized
Rising−55 mV0 mVActivatedPolarized → Depolarized
Rising0 mV+30 mVActivated → InactivatedDepolarized
Falling+30 mV0 mVInactivatedDepolarized → Repolarized
Falling0 mV−70 mVInactivatedRepolarized
Undershot−70 mV−75 mVInactivated → DeactivatedRepolarized → Hyperpolarized
Rebounding−75 mV−70 mVDeactivatedHyperpolarized → Polarized

when the neuron generates a nerve impulse, is caused by a sudden movement of ions across the membrane—specifically, a flux of Na+ into the cell. 

 It is important that the sodium concentration in the cytosol remain low: if it increases, the red blood cells will swell and then burst as water rushes in. As red blood cells pass through the lungs, they quickly gain oxygen because oxygen molecules can pass rapidly across the plasma membrane by simple diffusion

Unlike bacteria, most eukaryotic cells do not have an H+ electrochemical gradient across their plasma membranes. Rather, it is sodium ions that are more concentrated outside the cell than inside (Fig. 12.3). Typically, 

the sodium concentration in the cytosol is about 10 mmol liter−1 while the concentration in the extracellular medium is about 150 mmol liter−1.

The cytosol is between 70 and 90 mV more negative than the extracellular medium, that is, the transmembrane voltage of the plasma membrane is between −70 and −90 mV. There is therefore a large inward electrochemical gradient for sodium ions. If sodium ions are allowed to rush down this gradient, they release energy—approximately 15 kJ for every mole of Na+ entering the cytosol.

Consider what happens if a few sodium ions move out of the extracellular fluid and into the cytosol of a eukaryotic cell—for example, when a nerve cell transmits the electrical signal called an action potential (Chapter 15). The sodium gradient has been slightly depleted: the cell holds less of this energy currency than it did before. However, the cell still has plenty of energy in the form of ATP that it can convert into energy as a sodium gradient. It does this using the sodium/potassium ATPase. This protein is located in the plasma membrane. Its function is to move 3Na+ ions out of the cell and to move 2K+ ions into the cell. For this to happen ATP is hydrolyzed to ADP thus giving up energy that is used to push Na+ out of the cytosol to its higher energy state in the extracellular medium.


The sodium/potassium ATPase carries(hold) sodium and potassium ions, while both ATP synthase(A mitochondrial enzyme called ATP synthase is found in the inner membrane of mitochondria) and the electron transport chain carry H+ ions.

Ions are electrically charged. This fact has two consequences for membranes. First, the movement of ions across a membrane will tend to change the voltage across that membrane. If positive ions leave the cytosol, they will leave the cytosol with a negative voltage, and vice versa. Second, a voltage across a membrane will exert a force on all the ions present. If the cytosol has a negative voltage, then positive ions such as sodium and potassium will be attracted in from the extracellular medium.

Potassium Channels Make the Plasma Membrane Permeable to Potassium Ions The potassium channel (Fig. 14.1) is a protein found in the plasma membrane of almost all cells. It is a tube that links the cytosol with the extracellular fluid. Potassium ions, which cannot pass through the lipid bilayer of the plasma membrane, pass through the potassium.

The glucose carrier is present in the plasma membrane of all human cells. 6. The sodium/calcium exchanger is a carrier that uses the energy of the sodium gradient to push calcium ions out of the cell.

When the transmembrane voltage is −70 mV, the voltage-gated sodium channel is gated shut. 2. When the plasma membrane is depolarized, the channel opens rapidly and then, after about 1 ms, inactivates.


The membrane of squid axons contains voltage-gated sodium channels that, like ours, normally inactivate about 1 ms after they are opened by a depolarization( more Na+ in cell),

Like calcium, sodium is at a much higher concentration outside the cell than inside. In a mammal, the sodium concentration in the blood is 150 mmol liter−1, whereas in the cytosol it is 10 mmol liter−1. When voltage-gated sodium channels open, sodium ions rush into the cell carrying positive charge and depolarizing the plasma membrane. This then favors the opening of more voltage-gated sodium channels, and so on. This positive feedback produces a depolarization to +30 mV called the sodium action potential. Because the voltage-gated sodium channels inactivate so quickly, the sodium-based action potential lasts only for 1 ms.


Although enough sodium ions move into the cell to dramatically change the transmembrane voltage, the concentration of sodium ions inside the cell is increased only very slightly. The amount depends on the electrical capacitance of the cell membrane and the cell volume, but, for example, it can be calculated that a single sodium-based action potential increases the sodium concentration in the nerve cell axon of Figure 15.7 by only 250 nmol liter−1.


the plasma membrane then depolarizes rapidly (in this case as more and more sodium enters) until the transmembrane voltage is +30 mV. After only 1 ms, the voltage-gated sodium channels inactivate, and the transmembrane voltage returns to −70 mV, due to the action of the potassium channels.

The action potential has jumped from node to node in the extremely short time of 50 µs. Now sodium ions will rush into the node on the right, current will pass axially up the interior of the axon to the next node up, and in a further 50 µs the action potential will have jumped to the next node, and so on, all the way up to the proximal terminal at an overall speed of 20 m s−1.

 In the case of the pain receptor, these vesicles are filled with sodium glutamate. In response to the increased concentration of cytosolic calcium the regulated exocytotic vesicles move to the plasma membrane and fuse with it, releasing their contents into the extracellular medium.

When the channel is open, it allows sodium and potassium ions to pass through. The electrochemical gradient pushing sodium ions into the cell is much greater than the electrochemical gradient pushing potassium ions out of the cell. 

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