Acetyldigitoxin binds to a site on the extracellular aspect of the α-subunit of the Na<sup>+</sup>/K<sup>+</sup> ATPase pump in the membranes of heart cells (myocytes). This causes an increase in the level of sodium ions in the myocytes, which then leads to a rise in the level of calcium ions. The proposed mechanism is the following: inhibition of the Na<sup>+</sup>/K<sup>+</sup> pump leads to increased Na<sup>+</sup> levels, which in turn slows down the extrusion of Ca<sup>2+</sup> via the Na<sup>+</sup>/Ca<sup>2+</sup> exchange pump. Increased amounts of Ca<sup>2+</sup> are then stored in the sarcoplasmic reticulum and released by each action potential, which is unchanged by acetyldigitoxin. This is a different mechanism from that of catecholamines. Acetyldigitoxin also increases vagal activity via its central action on the central nervous system, thus decreasing the conduction of electrical impulses through the AV node. This is important for its clinical use in different arrhythmias. (en)
Toxicity includes ventricular tachycardia or ventricular fibrillation, or progressive bradyarrhythmias, or heart block. LD50 = 7.8 mg/kg (orally in mice). (en)