How is sodium-potassium pump regulated?

The activity of the sodium-potassium pump is regulated by catecholamines, steroid hormones, and peptide hormones. Short-term regulation involves direct effects on the kinetic behavior of the enzyme or translocation of sodium pumps between the plasma membrane and intracellular stores. Long-term regulatory mechanisms typically affect NA+-K+-ATPase synthesis or degradation. 

Steroid hormones, particularly corticosteroids, have specific long and short-term regulatory effects on the Na+-K+-ATPase. Long-term effects are typically regulated by alterations in mRNA/protein synthesis induced by direct interactions of receptor/corticosteroid complexes with DNA. Short-term effects may be mediated by specific membrane-associated receptors. 

Common catecholamines involved in sodium-pump regulation include dopamine and norepinephrine. A recent study has shown that PKC-mediated pathways may be involved in short-term responses to dopamine inhibition, and PKA may have a role in long-term responses. 

Insulin is the peptide hormone whose effects on the pump have been best characterized. One short-term effect of insulin on the pump is the translocation of sodium pumps from intracellular stores to the surface of the cell. Another short-term effect of insulin on the pump has been seen in the kidney as insulin increases the affinity of the enzyme for NA+.