Propranolol
Propranolol, sold under the brand name Inderal among others, is a medication of the beta blocker class. It is used to treat high blood pressure, a number of types of irregular heart rate, thyrotoxicosis, capillary hemangiomas, performance anxiety, and essential tremors. It is used to prevent migraine headaches, and to prevent further heart problems in those with angina or previous heart attacks. It can be taken by mouth or by injection into a vein. The formulation that is taken by mouth comes in short-acting and long-acting versions. Propranolol appears in the blood after 30 minutes and has a maximum effect between 60 and 90 minutes when taken by mouth.
Common side effects include nausea, abdominal pain, and constipation. It should not be used in those with an already slow heart rate and most of those with heart failure. Quickly stopping the medication in those with coronary artery disease may worsen symptoms. It may worsen the symptoms of asthma. Caution is recommended in those with liver or kidney problems. Propranolol may cause harmful effects in the baby if taken during pregnancy. Its use during breastfeeding is probably safe, but the baby should be monitored for side effects. It is a non-selective beta blocker which works by blocking β-adrenergic receptors.
Propranolol was patented in 1962 and approved for medical use in 1964. It is on the World Health Organization's List of Essential Medicines. Propranolol is available as a generic medication. In 2017, it was the 41st most commonly prescribed medication in the United States, with more than 17 million prescriptions.
Medical uses
Propranolol is used for treating various conditions, including:Cardiovascular
- Hypertension
- Angina pectoris
- Myocardial infarction
- Tachycardia associated with various conditions, including anxiety, panic, hyperthyroidism, and lithium therapy
- Portal hypertension, to lower portal vein pressure
- Prevention of esophageal variceal bleeding and ascites
- Anxiety
- Hypertrophic cardiomyopathy
Propranolol is not recommended for the treatment of high blood pressure by the Eighth Joint National Committee because a higher rate of the primary composite outcome of cardiovascular death, myocardial infarction, or stroke compared to an angiotensin receptor blocker was noted in one study.
Psychiatric
Propranolol is occasionally used to treat performance anxiety, although evidence to support its use in any anxiety disorders is poor. Its benefits appear similar to benzodiazepines in panic disorder with potentially fewer side effects such as addiction. Some experimentation has been conducted in other psychiatric areas:- Post-traumatic stress disorder and specific phobias
- Aggressive behavior of patients with brain injuries
- Treating the excessive drinking of fluids in psychogenic polydipsia
PTSD and phobias
Ethical and legal questions have been raised surrounding the use of propranolol-based medications for use as a "memory damper", including: altering memory-recalled evidence during an investigation, modifying behavioral response to past experiences, the regulation of these drugs, and others. However, Hall and Carter have argued that many such objections are "based on wildly exaggerated and unrealistic scenarios that ignore the limited action of propranolol in affecting memory, underplay the debilitating impact that PTSD has on those who suffer from it, and fail to acknowledge the extent to which drugs like alcohol are already used for this purpose."
Others
- Essential tremor. Evidence for use for akathisia however is insufficient
- Migraine and cluster headache prevention and in primary exertional headache
- Hyperhidrosis
- Proliferating infantile hemangioma
- Glaucoma
- Thyrotoxicosis by deiodinase inhibition
Contraindications
Propranolol may be contraindicated in people with:- Reversible airway diseases, particularly asthma or chronic obstructive pulmonary disease
- Slow heart rate
- Sick sinus syndrome
- Atrioventricular block
- Shock
- Severe low blood pressure
- Cocaine toxicity
Adverse effects
- Diabetes mellitus or hyperthyroidism, since signs and symptoms of hypoglycaemia may be masked
- Peripheral artery disease and Raynaud's syndrome, which may be exacerbated
- Phaeochromocytoma, as hypertension may be aggravated without prior alpha blocker therapy
- Myasthenia gravis, which may be worsened
- Other drugs with bradycardic effects
Pregnancy and lactation
Most β-blocking agents appear in the milk of lactating women. However, propranolol is highly bound to proteins in the bloodstream and is distributed into breast milk at very low levels. These low levels are not expected to pose any risk to the breastfeeding infant, and the American Academy of Pediatrics considers propranolol therapy "generally compatible with breastfeeding".
Overdose
In overdose propranolol is associated with seizures. Cardiac arrest may occur in propranolol overdose due to sudden ventricular arrhythmias, or cardiogenic shock which may ultimately culminate in bradycardic PEA.Interactions
Since beta blockers are known to relax the cardiac muscle and to constrict the smooth muscle, beta-adrenergic antagonists, including propranolol, have an additive effect with other drugs which decrease blood pressure, or which decrease cardiac contractility or conductivity. Clinically significant interactions particularly occur with:- Verapamil
- Epinephrine
- β2-adrenergic receptor agonists
- * Salbutamol, levosalbutamol, formoterol, salmeterol, clenbuterol etc.
- Clonidine
- Ergot alkaloids
- Isoprenaline
- Nonsteroidal anti-inflammatory drugs
- Quinidine
- Cimetidine
- Lidocaine
- Phenobarbital
- Rifampicin
- Fluvoxamine
Pharmacology
Pharmacodynamics
Propranolol is classified as a competitive non-cardioselective sympatholytic beta blocker that crosses the blood–brain barrier. It is lipid soluble and also has sodium channel blocking effects. Propranolol is a non-selective β-adrenergic receptor antagonist, or beta blocker; that is, it blocks the action of epinephrine and norepinephrine at both β1- and β2-adrenergic receptors. It has little intrinsic sympathomimetic activity, but has strong membrane stabilizing activity. Propranolol is able to cross the blood–brain barrier and exert effects in the central nervous system in addition to its peripheral activity.In addition to blockade of adrenergic receptors, propranolol has very weak inhibitory effects on the norepinephrine transporter and/or weakly stimulates norepinephrine release. Since propranolol blocks β-adrenoceptors, the increase in synaptic norepinephrine only results in α-adrenoceptor activation, with the α1-adrenoceptor being particularly important for effects observed in animal models. Therefore, it can be looked upon as a weak indirect α1-adrenoceptor agonist in addition to potent β-adrenoceptor antagonist. In addition to its effects on the adrenergic system, there is evidence that indicates that propranolol may act as a weak antagonist of certain serotonin receptors, namely the 5-HT1A, 5-HT1B, and 5-HT2B receptors. The latter may be involved in the effectiveness of propranolol in the treatment of migraine at high doses.
Both enantiomers of propranolol have a local anesthetic effect, which is normally mediated by blockade of voltage-gated sodium channels. Studies have demonstrated propranolol's ability to block cardiac, neuronal, and skeletal voltage-gated sodium channels, accounting for its known membrane stabilizing effect and antiarrhythmic and other central nervous system effects.
Mechanism of action
Propranolol is a non-selective beta receptor antagonist. It competes with sympathomimetic neurotransmitters for binding to receptors, which inhibits sympathetic stimulation of the heart. Blockage of neurotransmitter binding to beta 1 receptors on cardiac myocytes inhibits activation of adenylate cyclase, which in turn inhibits cAMP synthesis leading to reduced PKA activation. This results in less calcium influx to cardiac myocytes through voltage gated L-type calcium channels meaning there is a decreased sympathetic effect on cardiac cells, resulting in antihypertensive effects including reduced heart rate and lower arterial blood pressure.Pharmacokinetics
Propranolol is rapidly and completely absorbed, with peak plasma levels achieved about 1–3 hours after ingestion. More than 90% of the drug is found bound to plasma protein in the blood. Coadministration with food appears to enhance bioavailability. Despite complete absorption, propranolol has a variable bioavailability due to extensive first-pass metabolism. Hepatic impairment therefore increases its bioavailability. The main metabolite 4-hydroxypropranolol, with a longer half-life than the parent compound, is also pharmacologically active. Most of the metabolites are excreted in the urine.Propranolol is a highly lipophilic drug achieving high concentrations in the brain. The duration of action of a single oral dose is longer than the half-life and may be up to 12 hours, if the single dose is high enough. Effective plasma concentrations are between 10 and 100 mg/l. Toxic levels are associated with plasma concentrations above 2000 mg/l.
History
scientist James W. Black developed propranolol in the 1960s. It was the first beta-blocker effectively used in the treatment of coronary artery disease and hypertension. In 1988, Black was awarded the Nobel Prize in Medicine for this discovery. Propranolol was inspired by the early β-adrenergic antagonists dichloroisoprenaline and pronethalol. The key difference, which was carried through to essentially all subsequent beta blockers, was the inclusion of an oxymethylene group between the aryl and ethanolamine moieties of pronethalol, greatly increasing the potency of the compound. This also apparently eliminated the carcinogenicity found with pronethalol in animal models.Newer, more cardio-selective beta blockers are now used preferentially in the treatment of hypertension.