The pacemaker cells (e.g. in the sinoatrial node) do not maintain a stable resting membrane potential but instead depolarise spotaneously.
Restoration of ionic gradients and resting state
Sodium slowly leaks into the cell, although potassium diffuses out of the cell simultaneously the net effect is a gradual increase in membrane potential. This continues until the threshold potential is reached at about -40mV.
Mainly due to T-type calcium channels
Slower than rapid sodium channels, therefore gradient less steep than myocyte action potential.
Effectively phase 1 absent and phase 2 very brief, therefore repolarisation is a single phase.
Sodium and calcium pumped out and potassium is pumped in, this requires ATP.
How to alter pacemaker rate
If the threshold potential becomes less negative, it takes longer to reach and therefore pacemaker rate decreased. E.g. quinidine, procainamide.
If membrane potential becomes more negative then it takes longer to reach the threshold potential during phase 4.
Increased acetylcholine levels increase potassium efflux by altering the permeability of the membrane – this explains how increased vagal tone causes bradycardia.