Pacemakersejtek

Pacemakersejtek are specialized cardiac muscle cells that generate rhythmic electrical impulses and thereby set the heart’s rate and rhythm. They exhibit automaticity, allowing spontaneous depolarization during diastole to initiate each heartbeat.

In electrophysiology, pacemakersejtek display a pacemaker potential (phase 4) caused by inward currents through HCN channels that carry the If current, along with contributions from T-type calcium channels. The upstroke of the action potential in nodal cells is mainly calcium-driven via L-type calcium channels, rather than sodium-dependent. These cells have no stable resting membrane potential and a relatively reduced inward rectifier potassium current (IK1) compared with atrial or ventricular myocytes. This combination underlies their automatic, rhythmic firing.

Location and function: The primary cluster of pacemakersejtek resides in the sinoatrial node (SA node) in the right atrium, which serves as the natural pacemaker of the heart. Secondary pacemakers include the atrioventricular node and Purkinje fibers, which can assume pacing if SA node function is impaired, though often at a slower rate. Impulses generated by pacemakersejtek propagate through atrial myocardium to the atrioventricular node and onward to the ventricles.

Regulation: Pacemaker activity is modulated by the autonomic nervous system and circulating catecholamines. Sympathetic stimulation increases the slope of phase 4 depolarization via β-adrenergic receptors and higher cAMP, increasing heart rate; parasympathetic activity via acetylcholine slows the rate by reducing cAMP and If. Circadian and hormonal influences also affect pacemaker activity.

Clinical relevance: Dysfunction of pacemakersejtek can lead to bradyarrhythmias or sick sinus syndrome. In cases of inadequate SA node function, artificial pacemakers may be implanted to maintain a stable heart rhythm.