Final answer:
Kinase B would increase the time voltage-gated sodium channels remain open, extending depolarization. Potassium channel blockers affect the action potential's repolarization phase by impeding voltage-gated K+ channels, crucial for returning the membrane potential to resting state.
Step-by-step explanation:
If kinase A decreases voltage-gated sodium channel conductance, it would reduce the magnitude of sodium currents after their opening. In contrast, if kinase B slows the inactivation of voltage-gated sodium channels, you would expect kinase B to increase the duration that the sodium channels remain open, thereby prolonging the sodium influx and extending the depolarization phase of the action potential.
Potassium channel blockers, such as amiodarone and procainamide, affect the repolarization phase of the action potential by impeding the movement of K+ through voltage-gated K+ channels. The delayed opening and the delayed closing of these channels are crucial for restoring the membrane potential back to its resting state after an action potential, which is a vital aspect of electrochemical signaling in neuronal and cardiac tissues.