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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 “Ca 2+  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 Ca 2+  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 ([Ca 2+ ]  i  ) that we have acquired from these cells. The human SAN pacemaker cells have a smaller  I    f  , a weaker [Ca 2+ ]  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.

Calcium Transient and Sodium-Calcium Exchange Current in Human versus Rabbit Sinoatrial Node Pacemaker Cells