Is pacemaker action potential considered a calcium dependent or sodium/calcium dependent? Is a sinoatrial node action potential (AP) considered a Ca2+ dependent (No Na+) action potential? 
I was under the understanding that Ca2+ dependent APs were present only in Purkinje and endocrine cells, while cardiac and skeletal myocytes elicited Na+/Ca2+ dependent APs. But I am not sure which category sinoatrial node APs fall under.
The initiation of SA node action potential is through slow Na+ channels (slow, inward depolarising current, note there are no fast Na channels. These pacemaker setting Na channels only act when it is VERY hyperpolarised, won't initiate otherwise). As the membrane potential rises, you get the additional opening of T-type calcium channels and then the opening of L-type calcium channels. These all add to the depolarisation until you reach the threshold potential where an AP can then fire. I think some K+ channels also close during this early depolarisation.

During the action potential rising phase (after threshold), it is primarily L-type Ca channels that are bringing Ca into the cell (the other channels close off a bit). As you reach the peak of the action potential, the L-type channels close and the K+ dawgs open, causing the repolarisation phase. Also note that the speed in which Ca2+ can move in through L-type channels is somewhat compromised compared to other channels, so it's slower and causes that slower up/rising phase (which is what you want in a pacemaker cell - check out the link for the shape of the SA node AP).

http://cvphysiology.com/Arrhythmias/A004.htm