Propranolol | A Beta-Adrenergic Receptor Antagonist

On cardiac myocytes, including the sinoatrial and atrioventricular nodes, there are beta-1 receptors. These receptors are activated, which results in an increase in cyclic AMP and an increase in intracellular calcium. Increased muscle fiber contractility results from this mechanism. Beta-adrenergic receptor blockade causes the heart’s overall workload to be reduced, which in turn lowers oxygen consumption and causes myocardial remodeling. [8]
On the other hand, beta-2 receptor activation results in an increase in cyclic AMP, which activates protein kinase A and causes smooth muscle cells in many organs and arteries to relax. Therefore, there is a slight vasoconstriction when beta-2 receptors are inhibited. Due to this action, it can be difficult for asthmatics to administer emergency epinephrine since it prevents epinephrine from potentially binding to pulmonary receptors. [9] Beta-blockers have a Vd of approximately 4 to 6 L/kg and are well distributed throughout the body. They are also highly protein-bound.

Propranolol’s active metabolite, 4-hydroxypropranolol, is created via hydroxylation with the help of the CYP2D6 enzyme.
Additionally, propranolol, like the majority of ingested drugs, is primarily eliminated by the kidneys, having a half-life of between 3 and 6 hours in people with healthy renal systems.

You can administer propranolol intravenously or orally. Continuous ECG monitoring should be done while a gradual infusion is administered intravenously. This method of administration is most frequently used in inpatient settings.

The dosage of propranolol varies, mainly depending on the ailment it is used to treat.