Cardiac biological pacemaker (BP) has been created by suppression of the inward-rectifier K⁺ current (I_K1) or overexpression of the hyperpolarization-activated current (I_h). We theoretically investigated the effects of incorporating I_h, T-type Ca²⁺ current (I_Ca,T), sustained inward current (I_st) and/or low voltage-activated L-type Ca²⁺ current (I_Ca,LD) on 1) creation of BP cells, 2) robustness of BP activity to electrotonic loads of non-pacemaking (NP) cells, and 3) BP cell ability to drive NP cells. We used a single cell model for human ventricular myocytes (HVMs), and also coupled-cell models composed of BP and NP cells. Bifurcation structures of the model cells were explored during changes in conductance of the currents and gap junction. Incorporating the pacemaker currents did not yield BP activity in HVM with normal I_K1, but increased the critical I_K1 conductance for BP activity to emerge. Expressing I_h appeared to be most helpful in facilitating creation of BP cells via I_K1 suppression. In the coupled-cell model, I_st significantly enlarged the gap conductance (G_C) region where stable BP cell pacemaking and NP cell driving occur, reducing the number of BP cells required for robust pacemaking and driving. In contrast, I_h enlarged the G_C region of pacemaking and driving only when I_K1 of the NP cell was relatively low. I_Ca,T or I_Ca,LD exerted the effects similar to those of I_st, but caused shrinkage or irregularity of BP oscillations. These findings suggest that expressing I_st most effectively improves the structural stability of BPs to electrotonic loads and BP ability to drive the ventricle.