During the repolarization phase of the sa nodal cell action potentials, what is happening?

Action potential phases:

  Phase 0: Rapid depolarization
     - ↑ Na+ and ↓ K+ conductances

  Phase 1: Initial repolarization 
     - ↓ Na+ and ↑ K+ conductances

  Phase 2: Plateau phase
     - ↑ Ca++ conductance

  Phase 3: Repolarization
     - ↑ K+ and ↓ Ca++ conductances

  Phase 4: Resting potential     
     - ↑ K+ and ↓ Na+ and ↓ Ca++ conductances

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Antiarrhythmic drugs that affect the movement of these ions are used to alter cardiac action potentials in order to prevent or stop arrhythmias. In non-nodal tissue, sodium-channel blockers decrease the fast inward movement of Na+, thereby decreasing the slope of phase 0 and the magnitude of depolarization. The principal effect of this change is a reduction in conduction velocity. These drugs also increase the effective refractory period (ERP) by delaying the reactivation of fast-sodium channels. Potassium-channel blockers delay phase 3 repolarization, thereby lengthening the action potential duration and ERP.

Nodal Cell Action Potentials

Action potential phases:

  Phase 0: Depolarization
     - ↑ Ca++ and ↓ K+ conductances

  Phase 3: Repolarization 
     - ↑ K+ and ↓ Ca++ conductances

  Phase 4: Spontaneous depolarization
     - "Funny" currents (If) through slow inward Na+ channels
     - ↑ Ca++ and ↓ K+ conductances

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Like fast-response action potentials, changes in the membrane conductance to calcium and potassium ions alter slow-response action potentials. Calcium-channel blockers reduce the slope of phase 4, thereby decreasing the rate of spontaneous depolarization, which reduces the rate of pacemaker firing. These drugs also decrease the slope of phase 0, which slows conduction velocity within the AV node. The AV nodal ERP is also lengthened by calcium-channel blockers. Potassium-channel blockers delay phase 3 repolarization, thereby lengthening the action potential duration and ERP.

Revised 09/06/22

DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-making advice.

Cells within the sinoatrial (SA) node are the primary pacemaker site within the heart. These cells are characterized as having no true resting potential, but instead generate regular, spontaneous action potentials. Unlike non-pacemaker action potentials in the heart, and most other cells that elicit action potentials (e.g., nerve cells, muscle cells), the depolarizing current is carried into the cell primarily by relatively slow Ca++ currents instead of by fast Na+ currents. There are, in fact, no fast Na+ channels and currents operating in SA nodal cells. This results in slower action potentials in terms of how rapidly they depolarize. Therefore, these pacemaker action potentials are sometimes referred to as "slow response" action potentials.

The changes in membrane potential during the different phases are brought about by changes in the movement of ions (principally Ca++ and K+, and to a lesser extent Na+) across the membrane through ion channels that open and close at different times during the action potential. When a channel is opened, there is increased electrical conductance (g) of specific ions through that ion channel. Closure of ion channels causes ion conductance to decrease. As ions flow through open channels, they generate electrical currents that change the membrane potential.

In the SA node, three ions are particularly important in generating the pacemaker action potential. The role of these ions in the different action potential phases are illustrated in the above figure and described below:

• At the end of repolarization, when the membrane potential is very negative (about -60 mV), ion channels open that conduct slow, inward (depolarizing) Na+ currents. These currents are called "funny" currents and abbreviated as "If". These depolarizing currents cause the membrane potential to begin to spontaneously depolarize, thereby initiating Phase 4. As the membrane potential reaches about -50 mV, another type of channel opens, which increases gCa++. This channel is called transient or T-type Ca++ channel. As Ca++ enters the cell through these channels down its electrochemical gradient, the inward directed Ca++ currents further depolarize the cell. When the membrane depolarizes to about -40 mV, a second type of Ca++ channel opens, which further increases gCa++. These are the so-called long-lasting, or L-type Ca++ channels. Opening of these channels causes more Ca++ to enter the cell and to further depolarize the cell until an action potential threshold is reached (usually between -40 and -30 mV). It should be noted that a hyperpolarized state is necessary for pacemaker channels to become activated. Without the membrane voltage becoming very negative at the end of phase 3, pacemaker channels remain inactivated, which suppresses pacemaker currents and decreases the slope of phase 4. This is one reason why cellular hypoxia, which depolarizes the cell and alters phase 3 hyperpolarization, leads to a reduction in pacemaker rate (i.e., produces bradycardia). During Phase 4 there is also a slow decline in the outward movement of K+ as the K+ channels responsible for Phase 3 continue to close. This fall in K+ conductance (gK+) contributes to the depolarizing pacemaker potential.
• Phase 0 depolarization is primarily caused by increased gCa++ through the L-type Ca++ channels that began to open toward the end of Phase 4. The "funny" currents, and Ca++ currents through the T-type Ca++ channels, decline during this phase as their respective channels close. Because the movement of Ca++ through these channels into the cell is not rapid, the rate of depolarization (slope of Phase 0) is much slower than found in other cardiac cells (e.g., Purkinje cells).
• Repolarization occurs (Phase 3) as K+ channels open (increased gK+) thereby increasing the outward directed, hyperpolarizing K+ currents. At the same time, the L-type Ca++ channels become inactivated and close, which decreases gCa++ and the inward depolarizing Ca++ currents.

During depolarization, the membrane potential (Em) moves toward the equilibrium potential for Ca++, which is about +134 mV. During repolarization, g’Ca++ (relative Ca++ conductance) decreases and g’K+ (relative K+ conductance) increases, which brings Em closer toward the equilibrium potential for K+, which is about -96 mV). Therefore, the action potential in SA nodal cells is primarily dependent upon changes in Ca++ and K+ conductances as summarized below:

Em = g'K+ (-96 mV) + g'Ca++ (+134 mV)

Although pacemaker activity is spontaneously generated by SA nodal cells, the rate of this activity can be modified significantly by external factors such as by autonomic nerves, hormones, drugs, ions, and ischemia/hypoxia.

It is important to note that action potentials described for SA nodal cells are very similar to those found in the atrioventrcular (AV) node. Therefore, action potentials in the AV node, like the SA node, are determined primarily by changes in slow inward Ca++ and K+ currents, and do not involve fast Na+ currents. AV nodal action potentials also have intrinsic pacemaker activity produced by the same ion currents as described above for SA nodal cells.

Revised 01/25/21

DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-making advice.