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Phase 4 is associated with heart diastole so is called diastolic depolarization.
It is the duration of this slow diastolic depolarization which controls the cardiac chronotropism.
They are the so-called "funny" channels and are responsible for the phase 4 diastolic depolarization.
Because the pacemaker potential represents the non-contracting time between heart beats (diastole), it is also called the diastolic depolarization.
Also they slow down the spontaneous discharge frequency of automatic pacemakers by depressing the slope of diastolic depolarization.
Since the 1940s, the concept of diastolic depolarization, or "pacemaker potential", has become established; this mechanism is a characteristic distinctive of cardiac tissue.
The voltage region encompassed by this transition is commonly known as pacemaker phase, or slow diastolic depolarization or phase 4.
Conversely, the "If activation" hypothesis suggests that after action potential termination, If provides a slowly activating inward current predominating over decaying Ik, thus initiating slow diastolic depolarization.
There is now substantial evidence that also sarcoplasmic reticulum (SR) Ca-transients participate to the generation of the diastolic depolarization via a process involving the Na-Ca exchanger.
Activation of ß-adrenergic receptors results in cAMP-mediated phosphorylation of membrane proteins and increases in ICaL and in If the end result is an acceleration of the slow diastolic depolarization.
Acetylcholine also inhibits the hyperpolarization-activated "pacemaker" current If the "Ik decay" hypothesis65 proposes that pacemaker depolarization results from slow deactivation of the delayed rectifier current, Ik, which, due to a time-independent background inward current, causes diastolic depolarization.