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Slow Diastolic Depolarization

Q: How do the sympathetic and parasympathetic nervous systems affect slow diastolic depolarization?

Based on standard physiological principles: The sympathetic nervous system accelerates slow diastolic depolarization in SA node cells; norepinephrine increases SA nodal firing rate.The parasympathetic nervous system decreases SA nodal activity via acetylcholine. Direct modulation of the SDD rate specifically by the parasympathetic nervous system is mediated through hyperpolarization and reduced slope of pacemaker depolarization.

Depolarisatio diastolica lenta

For medical students2 min readUpdated 2026-10-10

Slow diastolic depolarization (SDD) is a critical physiological process responsible for the unique property of cardiac automaticity. It occurs in the pacemaker cells of the sinoatrial (SA) node during the relaxation phase and leads to the spontaneous generation of an electrical impulse.

LocalizationOccurs in the pacemaker cells of the sinoatrial (SA) node.

Ionic currentsDriven by the interplay of potassium, sodium, and calcium currents.

Membrane potentialThe maximum diastolic potential of pacemakers is around –60 mV.

AP featureSA node cells completely lack a plateau phase.

Role in Cardiac Automaticity

The heart's ability to independently generate a rhythm without external neural stimuli is called automaticity. The primary source of this automaticity is the sinoatrial (SA) node. It is within its pacemaker cells during diastole (relaxation) that a complex cascade of ionic shifts occurs. The combination of these shifts forms slow diastolic depolarization (SDD), which smoothly brings the membrane potential to threshold, triggering a new action potential.

Ionic Mechanisms of Depolarization

The SDD process is based on the precise interaction of several ionic currents that change in intensity throughout the inter-spike interval.

The underlying mechanisms include:

Decreased potassium permeability. During diastole, the cell membrane gradually loses its permeability to potassium ions ($K^+$). This leads to a progressive decline in the potassium equilibrium potential. Consequently, the overall membrane potential decreases (depolarization occurs).
Inward sodium and calcium currents. Against the background of falling potassium permeability, a continuous slow inward leak of sodium ions ($Na^+$) occurs during the inter-spike interval. Calcium ions ($Ca^{2+}$) contribute to a 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, more abrupt increase in inward $Na^+$ and $Ca^{2+}$ currents takes place. This final upstroke accelerates spontaneous depolarization of the pacemaker cell membrane.

Potential Characteristics and Cell Comparison

Due to the specific distribution of these ionic currents, the electrical properties of pacemaker cells differ markedly from working cardiomyocytes.

The maximum diastolic potential of SA node cells is significantly lower (i.e., less negative) than that of ventricular myocardial cells. While in working ventricular myocardium this value is approximately –90 mV, in the sinoatrial node it is only –60 mV.

The action potential (AP) of SA node cells exhibits several unique features:

Absence of a true resting membrane potential. The cell never remains in a stable electrical equilibrium; the membrane potential continuously fluctuates due to pacemaker activity (SDD).
Absence of a plateau phase. Unlike working cardiomyocytes, the action potential trace of SA node cells lacks the characteristic horizontal plateau phase.

Mnemonic

To remember ion dynamics during SDD: "Potassium flows out ever weaker, while Sodium and Calcium leak in ever stronger."

Frequently asked questions

What are the specific phases of the SA nodal pacemaker cell action potential?

The action potential of an SA node pacemaker cell consists of three main phases:

Phase 4 — Slow diastolic depolarization (spontaneous depolarization).
Phase 0 — Depolarization (upstroke).
Phase 3 — Repolarization (return of potential to baseline).

A hallmark of pacemaker cells is the complete absence of a plateau phase and a stable resting membrane potential.

How do the sympathetic and parasympathetic nervous systems affect slow diastolic depolarization?

Based on standard physiological principles:

The sympathetic nervous system accelerates slow diastolic depolarization in SA node cells; norepinephrine increases SA nodal firing rate.
The parasympathetic nervous system decreases SA nodal activity via acetylcholine.

Direct modulation of the SDD rate specifically by the parasympathetic nervous system is mediated through hyperpolarization and reduced slope of pacemaker depolarization.

In which cells does slow diastolic depolarization occur?

It occurs in the pacemaker cells of the sinoatrial (SA) node, driving their automaticity.

How does membrane permeability to potassium change during SDD?

During diastole, membrane permeability to potassium ions progressively decreases, leading to depolarization.

How does the membrane potential of pacemakers differ from working cardiomyocytes?

In SA node cells, it is less negative (–60 mV) compared to ventricular myocardial cells (–90 mV). Additionally, pacemakers lack a true resting membrane potential and a plateau phase.

Go deeper

Dynamics of the potassium equilibrium potential during diastole
Role of the slow inward sodium current during the inter-spike interval
Impact of calcium currents at the end of the SDD phase
Differences in action potential morphology between the SA node and ventricular myocardium