Cardiac action potential action potential (see phase 2, below) and is a fundamental step in cardiac excitation-contraction coupling. There are important physiological differences between the cells that spontaneously generate the action potential (pacemaker cells; e.g. SAN) and those that simply conduct it (non-pacemaker cells; e.g. ventricular myocytes). The specific differences in the types of ion channels expressed and mechanisms by which they are activated results in differences in the configuration of the action potential waveform, as shown in figure 2. The standard model used to understand the cardiac action potential is that of the ventricular myocyte. Outlined below are the five phases of
Cardiac glycoside 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 cardiac glycosides also function to decrease heart rate. For example, the ingestion of digoxin leads to increased cardiac output and decreased