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    which statement would be true of a membrane-bound protein that works in conjunction with a sodium–potassium pump during secondary active transport?


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    2.16: Sodium

    The Sodium-Potassium Pump

    Active transport is the energy-requiring process of pumping molecules and ions across membranes "uphill" - against a concentration gradient. To move these molecules against their concentration gradient, a carrier protein is needed. Carrier proteins can work with a concentration gradient (during passive transport), but some carrier proteins can move solutes against the concentration gradient (from low concentration to high concentration), with an input of energy. In active transport, as carrier proteins are used to move materials against their concentration gradient, these proteins are known as pumps. As in other types of cellular activities, ATP supplies the energy for most active transport. One way ATP powers active transport is by transferring a phosphate group directly to a carrier protein. This may cause the carrier protein to change its shape, which moves the molecule or ion to the other side of the membrane. An example of this type of active transport system, as shown in Figure below, is the sodium-potassium pump, which exchanges sodium ions for potassium ions across the plasma membrane of animal cells.

    How a sodium-potassium pump work

    The sodium-potassium pump system moves sodium and potassium ions against large concentration gradients. It moves two potassium ions into the cell where potassium levels are high, and pumps three sodium ions out of the cell and into the extracellular fluid.

    As is shown in Figure above, three sodium ions bind with the protein pump inside the cell. The carrier protein then gets energy from ATP and changes shape. In doing so, it pumps the three sodium ions out of the cell. At that point, two potassium ions from outside the cell bind to the protein pump. The potassium ions are then transported into the cell, and the process repeats. The sodium-potassium pump is found in the plasma membrane of almost every human cell and is common to all cellular life. It helps maintain cell potential and regulates cellular volume.

    A more detailed look at the sodium-potassium pump is available at http://www.youtube.com/watch?v=C_H-ONQFjpQ (13:53) and http://www.youtube.com/watch?v=ye3rTjLCvAU (6:48).

    The Electrochemical Gradient

    The active transport of ions across the membrane causes an electrical gradient to build up across the plasma membrane. The number of positively charged ions outside the cell is greater than the number of positively charged ions in the cytosol. This results in a relatively negative charge on the inside of the membrane, and a positive charge on the outside. This difference in charges causes a voltage across the membrane. Voltage is electrical potential energy that is caused by a separation of opposite charges, in this case across the membrane. The voltage across a membrane is called membrane potential. Membrane potential is very important for the conduction of electrical impulses along nerve cells.

    Because the inside of the cell is negative compared to outside the cell, the membrane potential favors the movement of positively charged ions (cations) into the cell, and the movement of negative ions (anions) out of the cell. So, there are two forces that drive the diffusion of ions across the plasma membrane—a chemical force (the ions' concentration gradient), and an electrical force (the effect of the membrane potential on the ions’ movement). These two forces working together are called an electrochemical gradient, and will be discussed in detail in "Nerve Cells" and "Nerve Impulses" concepts.

    2.16: Sodium

    Source : bio.libretexts.org

    Physiology, Sodium Potassium Pump

    The Na+ K+ pump is an electrogenic transmembrane ATPase first discovered in 1957 and situated in the outer plasma membrane of the cells; on the cytosolic side.[1][2] The Na+ K+ ATPase pumps 3 Na+ out of the cell and 2K+ that into the cell, for every single ATP consumed. The plasma membrane is a lipid bilayer that arranged asymmetrically, containing cholesterol, phospholipids, glycolipids, sphingolipid, and proteins within the membrane.[3][4] The Na+K+-ATPase pump helps to maintain osmotic equilibrium and membrane potential in cells.


    The Na+ K+ pump is an electrogenic transmembrane ATPase first discovered in 1957 and situated in the outer plasma membrane of the cells; on the cytosolic side.[1][2] The Na+ K+ ATPase pumps 3 Na+ out of the cell and 2K+ that into the cell, for every single ATP consumed. The plasma membrane is a lipid bilayer that arranged asymmetrically, containing cholesterol, phospholipids, glycolipids, sphingolipid, and proteins within the membrane.[3][4] The Na+K+-ATPase pump helps to maintain osmotic equilibrium and membrane potential in cells.

    The sodium and potassium move against the concentration gradients. The Na+ K+-ATPase pump maintains the gradient of a higher concentration of sodium extracellularly and a higher level of potassium intracellularly. The sustained concentration gradient is crucial for physiological processes in many organs and has an ongoing role in stabilizing the resting membrane potential of the cell, regulating the cell volume, and cell signal transduction.[2] It plays a crucial role on other physiological processes, such as maintenance of filtering waste products in the nephrons (kidneys), sperm motility, and production of the neuronal action potential.[5] Furthermore, the physiologic consequences of inhibiting the Na+-K+ ATPase are useful and the target in many pharmacologic applications. 

    Na, K-ATPase is a crucial scaffolding protein that can interact with signaling proteins such as protein kinase C (PKC) and phosphoinositide 3-kinase (PI3K).[6]


    Structurally, the Na+ K+ ATPase is composed of a catalytic alpha subunit and an auxiliary beta subunit.[7] Some Na-K ATPases include a subunit that is tissue-specific and belongs to the FXYD protein family.[8] The alpha subunit contains a transmembrane region which is composed of 10 helices, referred to as MA1-M10. Within these ten helices, ion binding sites, specifically three binding sites that bind to Na+ in the E1 state and two binding sites that bind to K+ in the E2 state.[9][10][11][12] The structure of the Na-K ATPase is composed of three sites. Site one and two overlap within both the E1 and E2 states. However, site three is exclusively in the E1 state and is between the M5, M6, and M8 transmembrane helices, which bind to Na+ and catalyze H+ transport as well,[13][14] dependent on the Na+, K+, and H+ concentrations.[15] According to previous studies, the pump’s E2 state selectivity for K+ may be due to ion binding pocket protonation.[16]


    Sodium and potassium gradients function in various organ systems' physiologic processes.[5] The kidneys have a high level of expression of the Na, K-ATPase, with the distal convoluted tubule expressing up to 50 million pumps per cell. This sodium gradient is necessary for the kidney to filter waste products in the blood, reabsorb amino acids, reabsorb glucose, regulate electrolyte levels in the blood, and to maintain pH.[17]

    Sperm cells also use the Na, K-ATPase, but they use a different isoform necessary for preserving fertility in males. Sperm needs the Na, K ATPase to regulate membrane potential and ions, which is necessary for sperm motility and the sperm’s acrosome functioning during penetration into the egg.[18]

    The brain also requires NA, K ATPase activity. Neurons need the Na, K ATPase pump to reverse postsynaptic sodium flux to re-establish the potassium and sodium gradients which are necessary to fire action potentials. Astrocytes also need Na, K ATPase pump to maintain the sodium gradient as the sodium gradient maintains neurotransmitter reuptake. Na, K ATPases in the gray matter consumes a significant amount of energy, up to three-quarters of energy is absorbed by Na, K ATPases in the gray matter while merely a quarter of the total energy gets utilized for protein synthesis and molecular synthesis.[19]


    The Na+-K+ ATPase plays a prominent role in thyroid pathophysiology. In hyperparathyroidism, there is an increase in heat intolerance, increased sweating, and increased weight loss due to the increased synthesis of Na+-K+ ATPase induced by the excessive thyroid hormone. This increased synthesis of Na+-K+ ATPase then increases basal metabolic rate, which then increases oxygen consumption, respiratory rate, body temperature, and calorigenesis.[20]

    Clinical Significance

    As the Na+-K+ ATPase is essential for maintaining various cellular functions, its inhibition could result in diverse pathologic states. Studies show that patients with heart failure have a 40% lower concentration of total Na, K-ATPase.[21] One significant clinical application is in cardiovascular pharmacology. For example, ouabain is a cardiac glycoside that inhibits the Na+-K+ ATPase by binding to the K+ site. Other cardiac glycosides such as digoxin and digitoxin directly inhibit the Na+-K+ ATPase.[22] This inhibition causes a buildup of excessive K+ extracellularly, and accumulation of excessive Na+ intracellularly as the Na+-K+ ATPase can no longer pump K+ into the cell or pump Na+ out of the cell. This buildup of intracellular Na+ hinders the concentration gradient that usually drives the Na+/Ca 2+ channel exchanger, which generally pumps Na+ into the cell and Ca 2+ out of the cell because the concentration gradient is not favorable for Na+ to enter the cell as excessive Na+ has built up intracellularly. This indirect inhibition of Na+/Ca 2+ exchange, therefore, causes a buildup of Ca 2+ intracellularly because the exchanger cannot allow Ca 2+ to exit the cell since it cannot accept Na+ into the cell. This increased intracellular Ca 2+ then increases cardiac contractility. This positive inotropy stimulates the vagus nerve, causing a decrease in heart rate. This physiology is clinically significant in the treatment of heart failure as it increases the contractility of the heart. It is also clinically significant in the treatment of atrial fibrillation as it decreases the conduction of the atrioventricular node and causes depression of the sinoatrial node.[23] Diuretic therapy has also been shown to reduce myocardial Na, K-ATPase when there is potassium loss. In contrast, angiotensin-converting enzyme inhibitors could stimulate the activity of the Na, K pump.[21]

    Another significant clinical application includes the effect of beta-adrenergic agonists in increasing the number of Na+/K+ ATPase channels; this is because beta-adrenergic agonists can enhance the gene expression of the Na+-K+-ATPase pump, which ultimately results in an increased quantity of the enzyme and therefore increased the activity of the enzyme. Because of this increased quantity of Na+/K+ ATPase, more potassium is pumped into the cell, causing a buildup of intracellular potassium. Therefore, extracellularly, this inward shift of potassium results in hypokalemia in the extracellular blood. Thus beta-adrenergic agonists can cause increased Na+ transport out of the cell as well. Increased Na+ transport extracellularly across alveolar epithelial cells for example, which would then cause lung liquid to follow this flow of Na+, ultimately stimulating lung liquid clearance.[24]]

    Insulin also causes clinically significant effects on the Na+/K+ ATPase. Insulin increases the number of Na+/K+ ATPase pumps in the membrane as well, this leads to an intracellular shift of potassium, causing hypokalemia in the extracellular space of the blood.[25]

    There are reports of abnormal expression levels, or activity of the Na+K+ pump in diabetes, hypertension, Alzheimer's disease, and in various tumors including glioblastoma, non-small cell lung carcinoma, breast cancer, melanoma, colorectal carcinoma, and bladder cancer.[26].

    Na+ K+-ATPase and its endogenous regulators, the endogenous cardiac steroids (ECS), play a role in the etiology of bipolar disorder and are a potential target for drug development for the treatment.[27]

     Both RNA and DNA viruses can directly affect Na, K-ATPase function, in particular, viral infections targeting the host cell components. Na, K-ATPase holds promise as an antiviral strategy to minimize the resistance to antiviral drugs and has been shown to be effective.[28] Cardiac glycosides inhibit cytomegalovirus (CMV) replication, with an additive effect when combined with antiviral drugs such as ganciclovir.[29] Cardiac glycosides can also be active on other DNA viruses such as herpes simplex virus (HSV) by inhibiting the expression of a viral gene.[30]

    There is evidence of a Na/K-ATPase oxidant amplification loop in the process of aging, obesity, and cardiovascular disease.[31]

    Review Questions


    Physiology, Sodium Potassium Pump

    Source : www.ncbi.nlm.nih.gov

    Active transport: primary & secondary overview (article)

    Electrochemical gradients and the membrane potential. Primary and secondary active transport. Na+/K+ pump.

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    Facilitated diffusion

    Active transport


    Electrochemical gradients

    Image depicting the charge and ion distribution across the membrane of a typical cell. Overall, there are more positive charges on the outside of the membrane than on the inside. The concentration of sodium ions is lower inside the cell than in the extracellular fluid, while the reverse is true for potassium ions.

    Active transport: moving against a gradient

    Primary active transport

    The sodium-potassium pump cycle

    Figure showing the transport cycle of the sodium-potassium pump.

    How the sodium-potassium pump generates a membrane potential

    Secondary active transport

    Diagram of a sodium-glucose cotransporter, which uses the energy stored in a sodium ion gradient to transport glucose "uphill" against its gradient. The cotransporter accomplishes this by physically coupling the transport of glucose to the movement of sodium ions down their concentration gradient.

    Simple diagram of a symporter (carrying two molecules in the same direction) and an antiporter (carrying two molecules in opposite directions).

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    Facilitated diffusion


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    Active transport: primary & secondary overview (article)

    Source : www.khanacademy.org

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