<unk> s affect the sodium-potassium ATPase pump in<unk>  muscle cells to alter their function. Normally, these sodium-potassium pumps move potassium ions in and sodium ions out.<unk> s, 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 regard to potassium ion movement, because both<unk> s 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 /. Thus, calcium ions are also not extruded and will begin to build up inside the cell as well. 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<unk> s also function to decrease heart rate. For example, the ingestion of digoxin leads to increased<unk>  output and decreased heart rate without significant changes in blood pressure; this quality allows it to be widely used medicinally in the treatment of<unk>  arrhythmias.<unk> s were identified as senolytics: they can selectively eliminate senescent cells which are more sensitive to the ATPase-inhibiting action due to cell membrane changes.
Cardiac glycoside
Phytosteroid
Insulin analog
Glucocorticoid
Steroid ester
Eoxin
Clofibride
Xenohormone