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The sodium-potassium pump is a crucial enzyme that regulates ion gradients across cell membranes, using ATP to transport Na+ and K+ ions. Its activity is modulated by endogenous factors like cAMP and exogenous substances such as hormones and drugs. In cardiac disease treatment, inhibitors like digoxin enhance heart muscle contractility by affecting this pump, demonstrating its significance in both cellular physiology and medical applications.
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The sodium-potassium pump uses energy from ATP to move ions against their concentration gradients
Binding and Phosphorylation
The pump binds intracellular Na+ ions and ATP, leading to phosphorylation and a conformational change
Ion Transport
The pump transports three Na+ ions out of the cell and two K+ ions into the cell
Dephosphorylation and Cycle Completion
Dephosphorylation restores the pump's original conformation, completing the cycle
The pump's activity is regulated by endogenous factors such as cAMP and exogenous substances like hormones and drugs
cAMP can enhance the pump's activity by upregulating the Na+/K+-ATPase enzyme
Gs-coupled GPCRs increase cAMP levels, while Gi-coupled GPCRs decrease cAMP levels, regulating the pump's activity
5-InsP7, produced by IP6K1, regulates the pump by promoting its endocytosis and degradation
Thyroid hormone can upregulate the expression of Na,K-ATPase mRNA in certain cells
Cardiac glycosides such as digoxin and ouabain can inhibit the pump, leading to increased intracellular Na+ levels and enhanced cardiac performance
Inhibition of the pump can affect the Na+/Ca2+ exchanger, leading to increased intracellular Ca2+ levels and stronger cardiac muscle contractions
Digoxin inhibits the pump, leading to an accumulation of intracellular sodium and increased availability of calcium, improving cardiac output in patients with heart failure
Jens Christian Skou's research led to the identification of the Na+,K+-ATPase enzyme, for which he was awarded the Nobel Prize in Chemistry in 1997