What enzyme does Digoxin inhibit to control heart muscle contraction?

Digoxin primarily inhibits the enzyme known as sodium-potassium ATPase (often referred to simply as sodium ATPase), which plays a crucial role in maintaining the balance of sodium and potassium ions across cell membranes. By inhibiting sodium-potassium ATPase, digoxin leads to an increase in intracellular sodium levels. This rise in sodium levels subsequently results in less sodium being exchanged for calcium through the sodium-calcium exchanger, which increases intracellular calcium levels. The increased calcium enhances contractility of the heart muscle, thus improving heart function.

While sodium ATPase is the key enzyme targeted by digoxin, the option that describes multiple ATPase enzymes is broader in scope. Digoxin does have effects that involve calcium and can affect calcium transport in the context of how it influences overall ion balance in cardiac cells. However, the essential action revolves around sodium-potassium ATPase's role in facilitating the effects that result in improved cardiac contraction.

In clinical discussions, understanding that digoxin modifies the influx of calcium via its influence on sodium levels elucidates how it enhances the contractility of the heart. This knowledge is critical for CSPT candidates, as it emphasizes the biochemical mechanisms at play in drug action and their implications for patient care.