Pacemaker (or autorhythmic)
cells account for a small minority of cells in the myocardium. The
rest (99%) are contractile cells that are responsible for pumping
the blood. Pacemaker cells are concentrated at two
‘nodes’: the sinoatrial node (SA node), located in the right atrium
near the superior vena cava; and the atrioventricular node (AV
node), located at the base of the right atrium near the junction of
the four heart chambers. They are unique because they can
spontaneously produce action potentials in rhythm to control the
heart beat. They do this because they exhibit a specialized
membrane potential- the
pacemaker potential.
The membrane potential in cardiac
cells is different from the rest of the body due to 3 reasons:
- An increased influx of
sodium (Na+)
- This is the main factor driving the pacemaker potential towards
threshold. Cardiac cells possess unique Na+ ion channels (‘funny
channels’) that open in response to hyperpolarisation. Therefore
after an action potential, these open and allow sodium to flow into
the cell, pushing the membrane potential towards the resting
potential for sodium (60mV)
- A decreased efflux of
potassium (K+)
- On top of the effect of sodium, potassium channels in the heart
begin to close during hyper polarisation (of the action potential).
This limits the amount of potassium that can leave the cell,
pushing the membrane potential up further.
- Calcium flow is much more
important.
- The pacemaker potential is the main
determinant of the heart rate. Because the pacemaker potential
represents the non-contracting time between heart beats (diastole),
it is also called the diastolic depolarization.
The amount of net inward current required to move the cell membrane
potential during the pacemaker phase is extremely small, in the
order of few pAs, but this net flux arises from time to time
changing contribution of several currents that flow with different
voltage and time dependence. Evidence in support of the active
presence of K+, Ca2+, Na+ channels
and Na+/K+ exchanger during the pacemaker
phase have been variously reported in the literature, but several
indications point to the “funny”(If) current as one of
the most important.[4](see funny current). There is now
substantial evidence that also sarcoplasmic reticulum (SR)
Ca2+-transients participate to the generation of the
diastolic depolarization via a process involving the Na–Ca
exchanger.
- The threshold potential
is the potential an excitable cell membrane, such as a myocyte,
must reach in order to induce an action potential. This
depolarization is caused by very small net inward currents of
calcium ions across the cell membrane, which gives rise to the
action potential.