Final answer:
Class II antiarrhythmic β-blockers work by binding to β-adrenergic receptors on the heart and blocking adrenaline, which reduces heart rate, decreases myocardial contraction, and causes vasodilation. Metoprolol specifically targets β1-receptors, while propranolol is nonselective. Overprescription can lead to serious adverse effects such as bradycardia.
Step-by-step explanation:
The mechanism of action of β-blockers, particularly those classified as Class II antiarrhythmics, involves binding to β-adrenergic receptors, which are G-protein-linked receptors on the heart muscle cells. When adrenaline (epinephrine) binds to these receptors, it typically causes an increase in heart rate and strength of contraction, as well as vasoconstriction. β-blockers such as metoprolol and propranolol prevent adrenaline from binding, thereby reducing heart rate (negative chronotropic effect), decreasing force of contraction (negative inotropic effect), and causing vasodilation. These effects help to manage conditions like hypertension, congestive heart failure, and reduce the risk of heart attacks.
Specifically, metoprolol targets the β1-receptor exclusively, which is primarily found in the heart, while propranolol is a nonselective blocker, affecting both β1 and β2 receptors found in the heart and bronchial smooth muscles. By blocking these β-receptors, β-blockers slow down the heart rate and reduce myocardial oxygen demand, thus providing an antiarrhythmic effect.
β-blockers can also lead to adverse effects if overprescribed, such as bradycardia or even heart stoppage, which highlights the importance of careful dosing. It's worth noting that while β-blockers act on the β-receptors, potassium channel blockers such as amiodarone function differently by affecting the potassium channels during the cardiac action potential, specifically prolonging the repolarization phase.