Digoxin increases myocardial contractility in heart failure. The intracellular event that directly mediates its positive inotropic effect is:
- A Inhibition of Na+/K+-ATPase, causing a small rise in intracellular Na+ that reduces Ca2+ extrusion via NCX ✓
- B Inhibition of phosphodiesterase type 3, raising cAMP
- C Opening of sarcoplasmic reticulum ryanodine receptors
- D Blockade of the slow inward calcium current
Explanation
Digoxin inhibits the alpha subunit of membrane Na+/K+-ATPase. The modest rise in intracellular sodium reduces the gradient driving the sodium-calcium exchanger, so less calcium leaves the cell and more is stored in the sarcoplasmic reticulum for release on the next beat. Phosphodiesterase inhibition describes milrinone, not digoxin, which is the key distractor to eliminate.
Reference: Katzung's Basic and Clinical Pharmacology, 16th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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