Propranolol

Propranolol belongs to the beta-blocker family. It is a non-selective beta-blocker: it blocks both beta-1 and beta-2 adrenergic receptors, and it also has membrane-stabilising properties that contribute to its antiarrhythmic effect. The heart’s beta-1 receptors are normally activated by adrenaline and noradrenaline. By blocking them, propranolol slows the heart rate and reduces the force of contraction, which lowers the heart’s workload.

Beta-1 receptors also control the release of renin by the kidney. By blocking them, propranolol lowers renin and, through this pathway, contributes to the fall in blood pressure. Because it is not cardioselective, it also acts on beta-2 receptors, found notably in the bronchi. This blockade can trigger bronchospasm, which is why propranolol remains contraindicated in asthma or a history of bronchospasm.

Propranolol has many approved indications. It treats hypertension and angina, prevents migraine, and is used in obstructive hypertrophic cardiomyopathy as well as in the period following a heart attack. It is also used in the management of phaeochromocytoma, in combination, and in essential tremor and infantile haemangioma. This broad list explains why the same medicine is prescribed in very different settings.

These situations seem far apart, but they share the same lever: reducing the overdrive of the adrenergic system. By slowing the heart and dampening the response to adrenaline, propranolol eases a heart short of oxygen, calms a tremor sustained by nerve stimulation and cuts part of the signal that feeds certain migraines. Depending on the indication, it is prescribed to control a day-to-day symptom or to prevent a cardiovascular event.

Propranolol comes as immediate-release tablets, prolonged-release capsules, an oral solution and an injectable form. Its absorption from the gut is almost complete, but its bioavailability does not exceed 20 to 30%, because the liver destroys a large part of it on first pass. The liver metabolises it via the CYP2D6 and CYP1A2 enzymes, and more marginally CYP2C19. Its half-life ranges from 3 to 6 hours for the immediate-release form and can reach 10 hours for the prolonged-release form.

Taking the tablet with a meal slightly increases its bioavailability, by reducing hepatic first-pass clearance. Regularity matters more than the exact time: a treatment taken each day at the same moment maintains a steady effect. A beta-blocker should never be stopped on one’s own initiative, because abrupt withdrawal can revive the symptoms the treatment was containing. Any dose change is decided with the doctor who follows the treatment.

Some effects appear fairly often. Sleep is frequently affected: difficulty falling asleep and nightmares are among the effects classified as common in the summary of product characteristics. Also found there are bradycardia, cold extremities that may progress to Raynaud’s phenomenon, along with tiredness and weariness. These effects stem directly from the medicine’s mode of action, which slows the heart and lowers adrenergic tone.

Digestive disturbances, nausea, vomiting and diarrhoea, remain uncommon. More rarely occur hallucinations, confusion, mood disorders, orthostatic hypotension, heart block or bronchospasm. Depression and hypoglycaemia are reported at an undetermined frequency. This last point calls for attention in people with diabetes: propranolol can mask the signs of hypoglycaemia, in particular tachycardia, prolong the response to insulin, and beta-blockers can also raise blood sugar.

Several combinations call for caution. With verapamil or diltiazem, two calcium channel blockers, the risk of severe hypotension, bradycardia and cardiac failure rises markedly. Anti-inflammatories such as ibuprofen or indometacin reduce the blood-pressure-lowering effect. Rizatriptan sees its exposure climb by 70 to 80%, which requires reducing its dose, while sympathomimetics such as adrenaline counter the action of the beta-blocker.

Propranolol is contraindicated in asthma or bronchospasm, bradycardia, cardiogenic shock, hypotension, second- or third-degree atrioventricular block, sick sinus syndrome, uncontrolled heart failure or Prinzmetal’s angina. Stopping clonidine while on a beta-blocker can trigger a surge of rebound hypertension, which imposes a precise order for withdrawing the treatments. Monitoring watches the heart rate and pressure, and remains attentive in people exposed to hypoglycaemia.

Propranolol acts beyond the heart. By blocking adrenergic signalling to the pineal gland, beta-blockers lower the night-time production of melatonin, the hormone that prepares sleep. This gland lies outside the barrier that protects the brain, so the blockade reaches it even with molecules that penetrate the nervous system little. This sheds light on a frequent complaint during treatment: lighter sleep and less restorative nights. A randomised controlled trial in hypertensive patients on a beta-blocker showed that melatonin supplementation each evening lengthened sleep time by about 37 minutes and improved its efficiency, without tolerance or rebound insomnia on stopping.

The body makes melatonin from tryptophan, an amino acid supplied by food, found in walnuts, almonds and pumpkin seeds. These same foods provide magnesium, as do oats and whole grains, and a banana readily rounds off an evening meal. But melatonin itself exists only in trace amounts in food, and the body normally produces most of it. When the beta-blocker curbs this night-time production, the plate alone does not fill the gap, and this is where a targeted intake makes sense, in addition to your treatment, never in its place.