Another mechanism as important as the funny current (through HCN channels) is forward mode sodium-calcium exchanger (NCX) current.

The currents thought to be responsible for spontaneous depolarization in the SA node are the funny current, T-type calcium current, forward mode NCX, and finally the L-type calcium current. A cartoon of the SA node action potential is attached here.

Let us consider the depolarizing currents one by one.

The funny current If , discovered by Dario Difrancesco is an inward current which opens upon hyperpolarization. It therefore satisfies the requirements for a pace-maker current, initiating depolarization. This current can set off the voltage-gated calcium and delayed rectifier potassium currents and explain the spontaneous oscillations in membrane potential in the SA node. This oscillatory behaviour of membrane conductances is termed the “membrane clock”. However, even complete blockade of If does not result in cardiac arrest, though slowing of the heart occurs.

The T-type calcium current does not make much of a contribution. (It is a low-voltage activated calcium current, and T stands for transient).

The next one is forward mode NCX - the sodium-calcium exchanger. It extrudes 1 calcium ion while allowing 3 sodium ions to enter - there by producing an inward current. Intracellular calcium for extrusion through NCX, is released by the sarcoplasmic reticulum - an event called diastolic calcium release or localized calcium release (LCR). Some researchers (Edward Lakatta for one) believe that spontaneous calcium release by the SR during phase 4 and extrusion of that calcium by NCX, thereby allowing a net inward sodium current is the fundamental pace-maker mechanism - they call this the calcium clock.

The current view is that both membrane and calcium clocks are entrained to produce the spontaneous AP in SA node.

The upstroke of the action potential (phase 0) is due the L-type calcium current (long-lasting, this is a high-voltage activated current).

The plasma membrane of each cardiomyocytes (the cellular level) is made with a phospholipids bilayer (which is an electrical insulator) and channels (which are conductive).

In the heart there are differents regions (atria, ventricules, sino atrial node, atrio-ventricular node, Purkinje fibers, ...) and each cardiomyocytes in these regions are constitutively different (they have differents channels and the quantity of these channels is different).

The natural pacemaker of the heart is located in the sinoatrial node (biological pacemaker, the other name is Keith and Flack node), on the right atria close to the superior veina cava. The cells in this node have a specific sodium channel named HCN (for Hyperpolarization-activated Cyclic Nucleotide gated). These channels are special because they are open by hyperpolarization (around -50 /-60mV). In this case at the end of the previous Action Potential, the transmembrane potential decrease to -50/-60mV because the potassium channels are open (repolarization, phase 4 of the previous AP), which activate the HCN channels (opening) leading an entrance of sodium and calcium which depolarize the cell (this current is named funny current or If and this is the diastolic depolarization).

It is the presence of the specific channels HCN which are responsible of the heart automaticity.

Complete sequence of an Sino atrial node action pacemaker :

The Action Potential (AP) in the Sinoatrial node is a calcic AP or slow answer. The resting potential of cells in Sinoatrial node is around -60mV, the threshold is around -40mV. The first ionic current which is the pacemaker of the heart rhythm is called I funny (If) because it is activated by hyperpolarization. This current is an inward current of Na+ and K+ at voltages below -40mV, mediated by HCN channels. This is the rapid phase 0 depolarization of the AP. When the membrane potential reaches the threshold (-40mV) the calcium can enters into the cell, this is the current ICa,T (for high threshold or tiny), and induces a very fast and high depolarization which is the phase 1 of AP. When the depolarization is at the maximum (+35mV) there is an outward current of depolarization mediated by three delayed rectifier currents K+ (IKr, IKs, and Ikur) using different channels: Ikr by HERG, Iks by KCNQ and KCNE and Ikur by Kv1.5 (Roden et al., 2002; Osteen et al., 2010). This is the phase 3 (the sinus node doesn't have phase 2 mediated by a long inward current calcium ICa,L).

http://physrev.physiology.org/content/88/3/919.full-text.pdf+html

Adding to Alexandre's excellent description, the rhythm that the SA node has can be thought of as an emergent property of the currents in and out of the cell. Broadly, the Ca current makes the voltage go up quickly, the K current makes the voltage go down quickly, and the funny current makes the voltage go up slowly.

The funny current turns on when the voltage is low enough, and slowly raises the voltage. When the voltage is high enough, the funny current turns off, and the Ca current turns on and very quickly raises the voltage. By making the voltage so high, the Ca current inactivates itself and turns on the K current. The K current brings the voltage back down again, turning itself off and the funny current on.

It's the way that these currents all work together that give the SA node its rhythm.

Another mechanism as important as the funny current (through HCN channels) is forward mode sodium-calcium exchanger (NCX) current.

The currents thought to be responsible for spontaneous depolarization in the SA node are the funny current, T-type calcium current, forward mode NCX, and finally the L-type calcium current. A cartoon of the SA node action potential is attached here.

Let us consider the depolarizing currents one by one.

The funny current If , discovered by Dario Difrancesco is an inward current which opens upon hyperpolarization. It therefore satisfies the requirements for a pace-maker current, initiating depolarization. This current can set off the voltage-gated calcium and delayed rectifier potassium currents and explain the spontaneous oscillations in membrane potential in the SA node. This oscillatory behaviour of membrane conductances is termed the “membrane clock”. However, even complete blockade of If does not result in cardiac arrest, though slowing of the heart occurs.

The T-type calcium current does not make much of a contribution. (It is a low-voltage activated calcium current, and T stands for transient).

The next one is forward mode NCX - the sodium-calcium exchanger. It extrudes 1 calcium ion while allowing 3 sodium ions to enter - there by producing an inward current. Intracellular calcium for extrusion through NCX, is released by the sarcoplasmic reticulum - an event called diastolic calcium release or localized calcium release (LCR). Some researchers (Edward Lakatta for one) believe that spontaneous calcium release by the SR during phase 4 and extrusion of that calcium by NCX, thereby allowing a net inward sodium current is the fundamental pace-maker mechanism - they call this the calcium clock.

The current view is that both membrane and calcium clocks are entrained to produce the spontaneous AP in SA node.

The upstroke of the action potential (phase 0) is due the L-type calcium current (long-lasting, this is a high-voltage activated current).

Plaese could you comment on effects of autoantibodies against heart proteins, and related (familial) illnesses?

Antonio, what is it that you want to know regarding autoantibodies and the heart?

Sinoatrial node  do not have a stable resting membrane potential. This membrane potential starts at about -60 mV and drifts upward, showing a gradual depolarization called WHAT? This results from a slow inflow of Na+ without a compensating outflow of K+.

https://www.inkling.com/read/anatomy-and-physiology-kenneth-saladin-6th/chapter-19/electrical-and-contractile

http://onlinelibrary.wiley.com/doi/10.1113/expphysiol.2011.060418/pdf