Role in cardiac automaticity
The ability of the heart to independently generate a rhythm without external nerve stimuli is called automaticity. The primary source of this automaticity is the sinoatrial (sinus) node. It is within its cells (pacemakers) during diastole—that is, during relaxation—that a complex cascade of ionic shifts occurs. The combination of these shifts forms slow diastolic depolarization (SDD), which smoothly shifts the membrane charge to the threshold level, triggering a new impulse.
Ionic mechanisms of depolarization
The SDD process is based on the strict interaction of several ionic currents that change their intensity throughout the interspike interval.
The underlying mechanisms are as follows:
- Decreased potassium permeability. During diastole, the cell membrane gradually loses its permeability to potassium ions ($K^+$). This leads to a predictable drop in the potassium equilibrium potential. As a result, the overall membrane potential decreases (depolarization occurs).
- Inward sodium and calcium currents. Against the background of falling potassium permeability, a slow inward current of sodium ions ($Na^+$) continuously exists inside the cell during the interspike interval. Calcium ions ($Ca^{2+}$) participate in this to a slightly lesser extent. The equilibrium potentials of sodium and calcium actively counteract the potassium potential, shifting the charge in the positive direction.
Toward the end of the SDD phase, an additional, sharper increase in the inward $Na^+$ and $Ca^{2+}$ current occurs. This final surge accelerates the spontaneous depolarization of the pacemaker cell membrane.
Potential characteristics and cell comparison
Due to the specific distribution of the described ionic currents, the electrical characteristics of pacemakers differ significantly from working cardiomyocytes.
The maximum membrane potential of sinus node cells is significantly lower (i.e., less negative) than that of ventricular myocardial cells. While this figure is at the level of –90 mV in the working ventricular myocardium, it is only –60 mV in the sinoatrial node.
The action potential (AP) of sinus node cells has a number of unique features:
- Absence of a resting potential. The cell is never in a stable electrical equilibrium; the membrane potential constantly changes due to pacemaker activity (SDD).
- Absence of a plateau. Unlike working cardiomyocytes, the action potential graph of sinus node cells lacks the characteristic horizontal plateau phase.
Briefly: answers to topical questions
What specific phases make up the action potential of a sinus node pacemaker cell?
The action potential of a sinoatrial node pacemaker cell consists of three main phases.
- Phase 4 — slow diastolic depolarization (spontaneous depolarization).
- Phase 0 — depolarization (sharp upstroke of potential).
- Phase 3 — repolarization (return of potential to baseline).
A distinctive feature of pacemaker cells is that they completely lack a plateau phase and also lack a stable resting potential.
How do the sympathetic and parasympathetic nervous systems affect the rate of slow diastolic depolarization?
According to the cited sources:
- The sympathetic nervous system accelerates slow diastolic depolarization in sinus node cells; norepinephrine increases sinoatrial node function.
- The parasympathetic nervous system decreases sinoatrial node function via acetylcholine.
There is no direct indication in the sources regarding a change specifically in the SDD rate under the influence of the parasympathetic nervous system.
To remember ion dynamics during SDD: "Potassium efflux gets progressively weaker, while Sodium and Calcium influx get progressively stronger."
Class and exam questions
In which cells does slow diastolic depolarization take place?
It occurs in the pacemaker cells of the sinoatrial (sinus) node, providing their automaticity.
How does membrane permeability to potassium change during SDD?
During diastole, membrane permeability to potassium ions gradually decreases, leading to depolarization.
How does the membrane potential of pacemakers differ from working cardiomyocytes?
In sinus node cells, it is less negative and equals –60 mV, whereas in ventricular myocardial cells it is –90 mV. Additionally, pacemakers lack a true resting potential and a plateau phase.
What else to study on this topic
- Dynamics of the potassium equilibrium potential during diastole
- The role of the slow inward sodium current during the interspike interval
- The role of calcium currents at the end of the SDD phase
- Differences in the action potential waveform between the sinus node and ventricular myocardium
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