There is an ongoing debate on the mechanism underlying the pacemaker activity of sinoatrial node (SAN) cells, focusing on the relative importance of the “membrane clock” and the “Ca2+ clock” in the generation of the small net membrane current that depolarizes the cell towards the action potential threshold. Specifically, the debate centers around the question whether the membrane clock-driven hyperpolarization-activated current, I
f, which is also known as the “funny current” or “pacemaker current,” or the Ca2+ clock-driven sodium-calcium exchange current, I
NaCa, is the main contributor to diastolic depolarization. In our contribution to this journal's “Special Issue on Cardiac Electrophysiology,” we present a numerical reconstruction of I
f and
I
NaCa in isolated rabbit and human SAN pacemaker cells based on experimental data on action potentials, I
f, and intracellular calcium concentration ([Ca2+]i) that we have acquired from these cells. The human SAN pacemaker cells have a smaller I
f, a weaker [Ca2+]i transient, and a smaller I
NaCa than the rabbit cells. However, when compared to the diastolic net membrane current, I
NaCa is of similar size in human and rabbit SAN pacemaker cells, whereas I
f is smaller in human than in rabbit cells.