what is the mechanism of action of cardiac glycosides
Cardiac glycoside Cardiac glycosides affect the sodium-potassium ATPase pump in cardiac muscle cells to alter their function.[1] 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.[8] 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.[9][10]
Vein Veins are less muscular than arteries and are often closer to the skin. There are valves in most veins to prevent backflow.
Bull riding The flank strap
Van der Waals equation is the volume of the container occupied by each particle (not the velocity of a particle), and k is the Boltzmann constant. It introduces two new parameters: a', a measure of the average attraction between particles, and b', the volume excluded from v by one particle.