Final answer:
Beta-blockers reduce the slope of the pacemaker potential and prolong the repolarization phase, leading to a decreased heart rate and contraction force. Potassium channel blockers prolong the action potential duration by impeding K+ movement through voltage-gated K+ channels, affecting repolarization. Sodium and potassium ion pumps are critical for restoring resting potential after an action potential.
Step-by-step explanation:
β-blockers, or beta-blockers, affect the action potential curve of pacemaker cells in the heart by decreasing the rate of phase 4 depolarization. These drugs bind to β-1 receptors in the heart which are normally stimulated by neurotransmitters like norepinephrine (NE), leading to an increase in heart rate. By blocking these receptors, beta-blockers effectively slow down the heart rate (HR) and reduce the force of the heart's contractions. This is because β-blockers prevent cAMP production, which otherwise increases the heart's electrical excitability and contractility. The most known effects in relation to action potentials are a decrease in the slope of the pacemaker potential and prolongation of the repolarization phase, ultimately leading to a lower heart rate and reduced cardiac output.
Potassium channel blockers, such as amiodarone and procainamide, have a different action mechanism compared to β-blockers. They impede the movement of K+ through voltage-gated K+ channels, particularly affecting the repolarization phase of the cardiac action potential. During repolarization, potassium channels normally allow K+ to exit the cell, which helps return the cell's membrane potential to its resting state. By blocking these channels, these drugs prolong the action potential duration and refractory period, which can help in treating cardiac dysrhythmias, but can also pose risks like increasing the likelihood of arrhythmias if misused.
The roles of potassium and sodium ion pumps are critical in restoring the resting potential after an action potential has occurred. These pumps help to re-establish the electrochemical gradient across the membrane that is necessary for the next action potential to be initiated. Specifically, the Na+/K+ transporter pumps three sodium ions out of the cell for every two potassium ions it brings in, which is pivotal for terminating the action potential and maintaining the resting membrane potential.