Final answer:
Hyperpolarization delays the ability of SA node cells to reach the threshold necessary for another action potential, effectively slowing down the heart rate as it requires a stronger stimulus to initiate depolarization. Parasympathetic stimulation contributes to this process through acetylcholine-induced potassium channel opening, which leads to hyperpolarization.
Step-by-step explanation:
Hyperpolarization of Sinoatrial (SA) node cells decreases the rate of spontaneous action potential generation because it increases the time it takes for the membrane potential to reach the threshold required to trigger an action potential. During the prepotential phase, a slow influx of sodium ions raises the membrane potential until it reaches this threshold. Following that, rapid depolarization and repolarization occur. Hyperpolarization is like taking a step back after the action potential, increasing the distance the membrane potential must travel to reach the threshold again. During hyperpolarization, the potassium channels remain open longer, allowing more potassium ions to leave the cell, which makes the inside of the membrane more negative. Because the voltage-gated sodium channels are inactivated and cannot open again during the absolute refractory period, this prevents immediate reactivation of an action potential.
Moreover, parasympathetic stimulation influences the heart rate by releasing acetylcholine (ACh), which opens potassium channels and causes the rate of spontaneous depolarization to slow down, which leads to hyperpolarization and a decreased heart rate. SA node cells, therefore, require a stronger stimulus to overcome the negative charge inside and to reach the threshold needed to initiate another action potential.