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Electrical discharge from this cardiomyocyte may be characterized by a slow smooth transition from the Maximum Diastolic Potential (MDP, -70 mV) to the threshold (-40 mV) for the initiation of a new AP event. The voltage region encompassed by this transition is commonly known as pacemaker phase, or slow diastolic depolarization or phase 4.
Because the pacemaker potential represents the non-contracting time between heart beats , it is also called the diastolic depolarization. The amount of net inward current required to move the cell membrane potential during the pacemaker phase is extremely small, in the order of few pAs, but this net flux arises from time to time changing ...
The voltage-gated potassium channels (K v) are activated by depolarization. The currents produced by these channels include the transient out potassium current I to1. This current has two components. Both components activate rapidly, but I to,fast inactivates more rapidly than I to, slow. These currents contribute to the early repolarization ...
Activation of β-adrenergic receptors results in cAMP-mediated phosphorylation of membrane proteins and increases in ICaL and in If the result is an acceleration of the slow diastolic depolarization. Under resting conditions, vagal tone prevails and variations in heart period are largely dependent on vagal modulation.
Since the 1940s, the concept of diastolic depolarization, or "pacemaker potential", has become established; this mechanism is a characteristic distinctive of cardiac tissue. [16] When the threshold is reached and the resulting action potential fires, a heartbeat results from the interactions; however, when this heartbeat occurs at an irregular ...
When, at the end of a sinoatrial action potential, the membrane repolarizes below the I f threshold (about −40/−50 mV), the funny current is activated and supplies inward current, which is responsible for starting the diastolic depolarization phase (DD); by this mechanism, the funny current controls the rate of spontaneous activity of ...
Conductive cells contain a series of sodium ion channels that allow a normal and slow influx of sodium ions that causes the membrane potential to rise slowly from an initial value of −60 mV up to about –40 mV. The resulting movement of sodium ions creates spontaneous depolarization (or prepotential depolarization). [1]
Impulses of the wave are delayed upon reaching the AV node, which acts as a gate to slow and to coordinate the electrical current before it is conducted below the atria and through the circuits known as the bundle of His and the Purkinje fibers—all which stimulate contractions of both ventricles.