Question

Describe the function of the sodium/potassium ATPase. a. What does the protein/molecule itself do?(3 points) b. How does the function of this one protein/molecule play a role in homeostasis of the whole body? Describe at least three specific, unique ways.

Answer 1

Function of the sodium/potassium ATPase: Na⁺/K⁺-ATPase. Enzyme is a solute pump that pumps sodium out of cells while pumping potassium into cells, both against their concentration gradients. This pumping is active and is important for cell physiology. Cells contain a relatively high concentration of potassium ions but low concentrations of sodium ions and the concentration of these ions on the two sides of the membrane are interdependent, but same carries ATP-ase pumps three sodium ions out of the cell for every two potassium ions pumped in. It’s also helps in maintaining resting potential, effect transport, and regulates cellular volume. It also functions as a signal transducer/integrator to regulate MAPK pathway, ROS, as well as intracellular calcium.

Ans a.

·         This carrier molecule/ protein sometimes helps to transfer a solute molecule across the lipid bilayer resembles an enzyme-substrate reaction, and in many ways carriers behave like enzymes. In contrast to ordinary enzyme-substrate reactions, however, the transported solute is not covalently modified by the carrier protein, but instead is delivered unchanged to the other side of the membrane.

·         The ATP-powered transport proteins are able to collect the free energy released during ATP hydrolysis and use it to move ions or other molecules uphill against a potential or concentration gradient.

·         The proton-pumping ATPase (H⁺-ATPase) of the plant plasma membrane generates the proton motive force across the plasma membrane that is necessary to activate most of the ion and metabolite transport.

Ans b: Potassium is the most abundant cation in the intracellular fluid, and maintaining the proper distribution of potassium across the cell membrane is critical for normal cell function. Long-term maintenance of potassium homeostasis is achieved by alterations in renal excretion of potassium in response to variations in intake. Potassium plays a key role in maintaining cell function. Almost all cells possess an Na⁺-K⁺-ATPase, which pumps Na⁺ out of the cell and K⁺ into the cell and leads to a K⁺ gradient across the cell membrane (K⁺_in>K⁺_out) that is partially responsible for maintaining the potential difference across the membrane. This potential difference is critical to the function of cells, particularly in excitable tissues, such as nerve and muscle. The body has developed numerous mechanisms for defense of serum K⁺. These mechanisms serve to maintain a proper distribution of K⁺within the body as well as regulate the total body K⁺ content. The kidney is primarily responsible for maintaining total body K⁺ content by matching K⁺ intake with K⁺ excretion. Adjustments in renal K⁺ excretion occur over several hours; therefore, changes in extracellular K⁺ concentration are initially buffered by movement of K⁺ into or out of skeletal muscle. The regulation of K⁺ distribution between the intracellular and extracellular space is referred to as internal K⁺ balance.

The most important factors regulating this movement under normal conditions are insulin and catecholamines.

1. After a meal, the postprandial release of insulin functions to not only regulate the serum glucose concentration but also shift dietary K⁺ into cells until the kidney excretes the K⁺ load re-establishing K⁺ homeostasis. These effects are mediated through insulin binding to cell surface receptors, which stimulates glucose uptake in insulin-responsive tissues through the insertion of the glucose transporter protein GLUT4. An increase in the activity of the Na⁺-K⁺-ATPase mediates K⁺ uptake. In patients with the metabolic syndrome or CKD, insulin-mediated glucose uptake is impaired, but cellular K⁺ uptake remains normal, demonstrating differential regulation of insulin-mediated glucose and K⁺ uptake.

2. Catecholamines regulate internal K⁺ distribution, with α-adrenergic receptors impairing and β-adrenergic receptors promoting cellular entry of K⁺. β₂-Receptor–induced stimulation of K⁺ uptake is mediated by activation of the Na⁺-K⁺-ATPase pump. These effects play a role in regulating the cellular release of K⁺ during exercise. Under normal circumstances, exercise is associated with movement of intracellular K⁺ into the interstitial space in skeletal muscle. Increases in interstitial K⁺ can be as high as 10–12 mM with severe exercise. Accumulation of K⁺ is a factor limiting the excitability and contractile force of muscle accounting for the development of fatigue.

3. Increases in interstitial K⁺ play a role in eliciting rapid vasodilation, allowing for blood flow to increase in exercising muscle. During exercise, release of catecholamines through β₂ stimulation limits the rise in extracellular K⁺ concentration that otherwise occurs as a result of normal K⁺release by contracting muscle. Although the mechanism is likely to be multifactorial, total body K⁺ depletion may blunt the accumulation of K⁺ into the interstitial space, limiting blood flow to skeletal muscle and accounting for the association of hypokalemia with rhabdomyolysis.

4. Changes in plasma toxicity and acid–base disorders also influence internal K⁺balance. Hyperglycemia leads to water movement from the intracellular to extracellular compartment. This water movement favors K⁺ efflux from the cell through the process of solvent drag. In addition, cell shrinkage causes intracellular K⁺ concentration to increase, creating a more favorable concentration gradient for K⁺ efflux. Mineral acidosis, but not organic acidosis, can be a cause of cell shift in K⁺. As recently reviewed, the general effect of acidemia to cause K⁺ loss from cells is not because of a direct K⁺-H⁺ exchange, but, rather, is because of an apparent coupling resulting from effects of acidosis on transporters that normally regulate cell pH in skeletal muscle.