<Li> Drimia maritima (squill): proscillaridine A </Li> <Li> Bufo marinus (cane toad): various bufadienolides </Li> <P> Cardiac glycosides affect the sodium - potassium ATPase pump in cardiac muscle cells to alter their function . Normally, these sodium - potassium pumps move potassium ions in and sodium ions out . Cardiac glycosides, however, inhibit this pump by stabilizing it in the E2 - P transition state, so that sodium cannot be extruded: intracellular sodium concentration therefore increases . With regards to potassium ion movement, because both cardiac glycosides and potassium compete for binding to the ATPase pump, changes in extracellular potassium concentration can potentially lead to altered drug efficacy . Nevertheless, by carefully controlling the dosage, such adverse effects can be avoided . Continuing on with the mechanism, raised intracellular sodium levels inhibit the function of a second membrane ion exchanger, NCX, which is responsible for pumping calcium ions out of the cell and sodium ions in at a ratio of 3Na / Ca . Thus, calcium ions are also not extruded and will begin to build up inside the cell as well . </P> <P> The disrupted calcium homeostasis and increased cytoplasmic calcium concentrations cause increased calcium uptake into the sarcoplasmic reticulum (SR) via the SERCA2 transporter . Raised calcium stores in the SR allow for greater calcium release on stimulation, so the myocyte can achieve faster and more powerful contraction by cross-bridge cycling . The refractory period of the AV node is increased, so cardiac glycosides also function to decrease heart rate . For example, the ingestion of digoxin leads to increased cardiac output and decreased heart rate without significant changes in heart rate or blood pressure; this quality allows it to be widely used medicinally in the treatment of cardiac arrhythmias . </P>

What is the mechanism of action of cardiac glycosides
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