Sinoatrial Node Action Potentials why its called primary pacemaker

Sinoatrial Node Action Potentials

Cells within the sinoatrial (SA) node are the primary pacemaker site within the heart. These cells are characterized as having no true resting potential, but instead generate regular, spontaneous action potentials. Unlike most other cells that elicit action potentials (e.g., nerve cells, muscle cells), the depolarizing current is carried primarily by relatively slow, inward Ca++ currents instead of by fast Na+ currents. There are, in fact, no fast Na+ currents operating in SA nodal cells.
SA nodal action potentials are divided into three phases.
Phase 0 depolarization is primarily due to increased gCa++ (Ca++ conductance). Because the movement (or conductance) of Ca++ through their channels is not rapid (hence, the term "slow inward Ca++ channels"), the rate of depolarization (slope of Phase 0) is much slower than found in other cardiac cells (e.g., Purkinje cells).

  • Repolarization occurs (Phase 3) as gK+ increases and gCa++ decreases. 
  • Spontaneous depolarization (Phase 4) is due to a fall in gK+ as potassium channels close and to a small increase in gCa++. A slow inward Na+ current also contributes to Phase 4, and is thought to be responsible for what is termed the pacemaker or "funny" current (If). Once this spontaneous depolarization reaches threshold (about -40 mV), a new action potential is triggered. 

During depolarization, the membrane potential (Em) moves toward the equilibrium potential for Ca++, which is about +134 mV. During repolarization, gCa++ (relative Ca++ conductance) decreases and gK+ (relative K+ conductance) increases, which brings Em closer toward the equilibrium potential for K+. Therefore, the action potential in SA nodal cells is primarily dependent upon changes in Ca++ and K+ conductances as summarized below and in the above figure:

Em = g'K+ (-96 mV) + g'Ca++ (+134 mV)

Although pacemaker activity is spontaneously generated by SA nodal cells, the rate of this activity can be modified significantly by external factors such as by autonomic nerves, hormones, drugs, ions, and ischemia/hypoxia.
Regulation of Pacemaker Activity
The SA node displays intrinsic automaticity (spontaneous pacemaker activity) at a rate of 100-110 action potentials ("beats") per minute. This intrinsic rhythm is primarily influenced by autonomic nerves, with vagal influences being dominant over sympathetic influences at rest. This "vagal tone" brings the resting heart rate down to 60-80 beats/min.

The SA node is predominantly innervated by efferent branches of the right vagus nerves, although some innervation from the left vagus is often observed. Experimental denervation of the right vagus to the heart leads to an abrupt increase in SA nodal firing rate if the resting heart rate is below 100 beats/min. A similar response is noted when a drug such as atropine is administered. This drug blocks vagal transmission at the SA node by antagonizing the muscarinic receptors that bind to acetylcholine, which is the neurotransmitter released by the vagus nerve.
Parasympathetic (vagal) activation, which releases acetylcholine (ACh) onto the SA node, decreases pacemaker rate by increasing gK+ and decreasing slow inward gCa++ and gNa+; the pacemaker current (If) is suppressed.

These ionic conductance changes decrease the slope of phase 4 of the action potential, thereby increasing the time required to reach threshold. Vagal activity also hyperpolarizes the pacemaker cell during Phase 4, which results in a longer time to reach threshold voltage.
To increase heart rate, the autonomic nervous system increases sympathetic outflow to the SA node, with concurrent inhibition of vagal tone. Inhibition of vagal tone is necessary for the sympathetic nerves to increase heart rate because vagal influences inhibit the action of sympathetic nerve activity. Sympathetic activation, which releases norepinephrine (NE), increases pacemaker rate by decreasing gK+ and increasing slow inward gCa++ and gNa+; the pacemaker current (If) is enhanced. These changes increase the slope of phase 4.
Pacemaker activity is also altered by hormones. For example, hyperthyroidism induces tachycardia and hypothyroidism induces bradycardia. Circulating epinephrine causes tachycardia by a mechanism similar to norepinephrine released by sympathetic nerves.

Changes in the serum concentration of ions, particularly potassium, can cause changes in SA nodal firing rate.Hyperkalemia induces bradycardia or can even stop SA nodal firing. Hypokalemia increases the rate of phase 4 depolarization and causes tachycardia. It apparently does this by decreasing gK during phase 4.

Cellular hypoxia (usually due to ischemia) depolarizes the membrane potential causing bradycardia; severe hypoxia completely stops pacemaker activity.
Various drugs used as antiarrhythmics also affect SA nodal rhythm. Calcium-channel blockers, for example, cause bradycardia by inhibiting the slow inward Ca++ currents during phase 4 and phase 0. Drugs affecting autonomic control or autonomic receptors (e.g., beta-blockers, muscarinic antagonists) directly or indirectly alter pacemaker activity. Digitalis causes bradycardia by increasing parasympathetic (vagal) activity on the SA node; however, at toxic concentrations, digitalis increases automaticity and therefore can cause tachyarrhythmias.This toxic effect is related to the inhibitory effects of digitalis on the membrane Na+/K+-ATPase, which leads to cellular depolarization, increased intracellular calcium, and changes in ion conductances.