Final answer:
Acetylcholine can depolarize or hyperpolarize cardiac cells depending on the type of receptor it binds to. Nicotinic receptors cause depolarization, while muscarinic receptors can lead to depolarization or hyperpolarization.
Step-by-step explanation:
When acetylcholine binds to receptors on a cardiac cell, it can either polarize, depolarize, or hyperpolarize the cell. The specific effect depends on the type of receptor. If acetylcholine binds to a nicotinic receptor, it will depolarize the cell because these receptors are cation channels and allow positively charged sodium ions (Na+) to rush into the cell. In contrast, if acetylcholine binds to a muscarinic receptor, it might cause either depolarization or hyperpolarization depending on the specific variant of the receptor present on the cardiac cell.
In the autonomic system’s ganglionic neurons, which include both sympathetic and parasympathetic ganglia, acetylcholine released from preganglionic fibers activates neurons through nicotinic receptors, causing depolarization. However, cardiac conductive cells do not have a stable resting potential and rely on the influx of various ions, including sodium (Na+), potassium (K+), and calcium (Ca2+), to generate the prepotential phase and eventual depolarization during action potentials.