Final answer:
Local anesthetics like a newly developed one that blocks Na⁺ channels prevent the rapid depolarization during the action potential, decreasing the rate of rise of the upstroke. Lidocaine operates similarly, leading to temporary sensory and possibly motor paralysis. Potassium channel blockers have a different mechanism, prolonging repolarization in heart treatments.
Step-by-step explanation:
A newly developed local anesthetic that blocks Na⁺ channels in nerves is expected to decrease the rate of rise of the upstroke of the action potential. Blocking sodium channels prevents the influx of Na⁺ ions, thus inhibiting the rapid depolarization that is characteristic of the action potential's ascending limb. It would not shorten the absolute refractory period, abolish the hyperpolarizing after-potential, or alter the Na⁺ equilibrium potential.
Lidocaine and similar local anesthetics achieve their numbing effect by inhibiting the initiation and transmission of nerve impulses. Such drugs are crucial for medical procedures as they allow for painless interventions by temporarily blocking sensation.
Potassium channel blockers, on the other hand, affect a different part of the action potential. By impeding the movement of K⁺ through voltage-gated K⁺ channels, potassium channel blockers prolong the repolarization phase, which could have therapeutic effects on abnormal electrical activity in the heart.