Cardiac autorhythmic cells in the intrinsic conduction system generate action potentials that spread in waves to all the cardiac contractile cells. This action causes a coordinated heart contraction. Of all the cells in the body, only heart cells are able to contract on their own without stimulation from the nervous system. In this magnified view of the heart, we see an autorhythmic cell adjacent to several cardiac contractile cells. Action potentials generated by autorhythmic cells create waves of depolarization that spread to contractile cells via gap junctions. Autorhythmic cells begin depolarizing due to a slow continuous influx of sodium and reduced efflux of potassium. As sodium ions enter the cell, the inner surface of the plasma membrane gradually becomes less negative, generating the pacemaker potential. When the membrane potential gets to -40 mV, it has reached the threshold for initiating an action potential. Fast calcium channels open and positively charged calcium ions rush into the cell. Notice on the graph that the calcium influx produces the rapidly rising phase of the action potential depolarization, which results in the reversal of the membrane potential from negative to positive inside the cell. This reversal of membrane potential triggers the opening of potassium channels, resulting in potassium rapidly leaving the cell. Let’s observe the potassium efflux and the resulting repolarization. The potassium efflux produces repolarization, bringing the membrane potential back down to its resting level. Although not shown here, several other events take place during repolarization. Ionic pumps actively transport calcium back to the extra cellular space, while sodium/potassium pumps transport sodium out of the cell and bring potassium into the cell, thereby restoring ion concentrations to their resting levels. During the depolarization in adjacent autorhythmic cells or contractile cells, a few positive ions move through the gap junctions into neighboring contractile cells. This entry of positive ions brings the membrane potential to threshold, triggering voltage-gated channels and initiates depolarization.