Ventricular and Atrial Myocytes:
The cellular mechanism of myocyte contraction following electrical stimulation is too complex to become fully addressed in this section, but excellent discussions of electromechanical coupling could be found. Briefly, when the myocyte is stimulated, sodium channels about the cell surface membrane (sarcolemma) open, and sodium ions (Na+) circulation down their electrochemical gradient into the cell.
This sudden inward surge of ions is responsible for the sharp upstroke from the myocyte action potential (stage 0). A plateau stage follows during which the cell membrane potential remains relatively unchanged owing to the inward flow of calcium ions (Ca2+) and the outward flow of potassium ions (K+) through a number of various specialized potassium channels.
Repolarization occurs due to continued outward flow of K+ following inward flux of Ca2+ has stopped. Within the cell, the alter in membrane potential from the sudden influx of Na+ and the subsequent increase in intracellular Ca2+ causes the sarcoplasmic reticulum to discharge big numbers of calcium ions via specific Ca2+ discharge channels. The exact signaling mechanism is not recognized.
Once in the cytoplasm, however, Ca2+ released from the sarcoplasmic reticulum binds with the regulatory proteins troponin and tropomyosin. Myosin and actin are then allowed to interact and also the cross-bridges in between them bend, giving rise to contraction.
The procedure of relaxation is poorly understood also but appears to involve return of Ca2+ towards the sarcoplasmic reticulum via two transmembrane sarcoplasmic reticulum-embedded proteins: Ca2+-ATPase and phospholamban. Reuptake of Ca2+ is an active procedure that demands adenosine triphosphate (ATP).
The action potential of pacemaker cells is various from that described for ventricular and atrial myocytes. Quick sodium channels are absent, to ensure that rapid phase 0 depolarization is not observed in SA nodal and AV nodal cells. In addition, these cells are characterized by elevated automaticity from a relatively rapid spontaneous phase 4 depolarization.
A mixture of reduced outward circulation of K+ and inward flow of Na+ and Ca2+ by way of specialized channels seems to become responsible for this dynamic change in membrane possible. Myofibrils are sparse, even though present, in the specialized pacemaker tissue.