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Adrenergic blocking drugs also known as Beta blockers (sometimes written as β-blockers) are a class of drugs used for various indications, but particularly for the management of cardiac arrhythmias and cardioprotection after myocardial infarction. Whilst once first-line treatment for hypertension, their role was downgraded in June 2006 in the United Kingdom to fourth-line as they do not perform as well as other drugs, particularly in the elderly, and there is increasing evidence that the most frequently used beta-blockers at usual doses carry an unacceptable risk of provoking type 2 diabetes.[1]

Beta blockers may also be referred to as beta-adrenergic blocking agents, beta-adrenergic antagonists, or beta antagonists.


Beta blockers block the action of endogenous catecholamines (epinephrine (adrenaline) and norepinephrine (noradrenaline) in particular), on β-adrenergic receptors, part of the sympathetic nervous system which mediates the "fight or flight" response.

There are three known types of beta receptor, designated β1, β2 and β3. β1-Adrenergic receptors are located mainly in the heart and in the kidneys. β2-Adrenergic receptors are located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle. β3-receptors are located in fat cells.

β-Receptor antagonism

Stimulation of β1 receptors by epinephrine induces a positive chronotropic and inotropic effect on the heart and increases cardiac conduction velocity and automaticity. Stimulation of β1 receptors on the kidney causes renin release. Stimulation of β2 receptors induces smooth muscle relaxation (resulting in vasodilation and bronchodilation amongst other actions), induces tremor in skeletal muscle, and increases glycogenolysis in the liver and skeletal muscle. Stimulation of β3 receptors induces lipolysis.

Beta blockers inhibit these normal epinephrine-mediated sympathetic actions, but have minimal effect on resting subjects. That is, they reduce the effect of excitement/physical exertion on heart rate and force of contraction, dilation of blood vessels and opening of bronchi, and also reduce tremor and breakdown of glycogen.

It is therefore somewhat unexpected that non-selective beta blockers have an antihypertensive effect, since they appear to cause vasoconstriction. The antihypertensive mechanism appears to involve: reduction in cardiac output (due to negative chronotropic and inotropic effects), reduction in renin release from the kidneys, and a central nervous system effect to reduce sympathetic activity.

Antianginal effects result from negative chronotropic and inotropic effects, which decrease cardiac workload and oxygen demand.

The antiarrhythmic effects of beta blockers arise from sympathetic nervous system blockade – resulting in depression of sinus node function and atrioventricular node conduction, and prolonged atrial refractory periods. Sotalol, in particular, has additional antiarrhythmic properties and prolongs action potential duration through potassium channel blockade.

Blockade of the sympathetic nervous system on renin release leads to reduced aldosterone via the renin angiotensin aldosterone system with a resultant decrease in blood pressure due to decreased sodium [and H20] retention.

Intrinsic sympathomimetic activity

Some beta blockers (e.g. oxprenolol and pindolol) exhibit intrinsic sympathomimetic activity (ISA). These agents are capable of exerting low level agonist activity at the β-adrenergic receptor while simultaneously acting as a receptor site antagonist. These agents, therefore, may be useful in individuals exhibiting excessive bradycardia with sustained beta blocker therapy.

Agents with ISA are not used post-myocardial infarction as they have not been demonstrated to be beneficial. They may also be less effective than other beta blockers in the management of angina and tachyarrhythmia (Rossi, 2006).

α1-Receptor antagonism

Some beta blockers (e.g. labetalol and carvedilol) exhibit mixed antagonism of both β- and α1-adrenergic receptors, which provides additional arteriolar vasodilating action.

Other effects

Beta blockers decrease nocturnal melatonin release, perhaps partly accounting for sleep disturbance caused by some agents (Stoschitzky et al., 1999). Beta blockers protect against social anxiety.[Citation needed]

Clinical use

Large differences exist in the pharmacology of agents within the class, thus not all beta blockers are used for all indications listed below.

Indications for beta blockers include:

Beta blockers have also been used in the following conditions:

  • Hypertrophic obstructive cardiomyopathy
  • Acute dissecting aortic aneurysm
  • Marfan syndrome (chronic treatment with propranolol slows progression of aortic dilation and its complications)
  • Prevention of variceal bleeding in portal hypertension
  • Possible mitigation of hyperhidrosis

Congestive heart failure

Although beta blockers were once contraindicated in congestive heart failure, as they have the potential to worsen the condition, studies in the late 1990s showed their positive effects on morbidity and mortality in congestive heart failure (Hjalmarson, 2000; Leizorovicz, 2002; Packer, 2002). Bisoprolol, carvedilol and sustained-release metoprolol are specifically indicated as adjuncts to standard ACE inhibitor and diuretic therapy in congestive heart failure.

Anxiety and performance enhancement

Some people, particularly musicians, use beta blockers to avoid stage fright and tremor during public performance and auditions. The physiological symptoms of the fight/flight response associated with performance anxiety and panic (pounding heart, cold/clammy hands, increased respiration, sweating, etc.) are significantly reduced, thus enabling anxious individuals to concentrate on the task at hand.

Currently, no beta blocker is approved for anxiolytic use by the U.S. Food and Drug Administration. Still, use of beta blockers to combat the physical symptoms of anxiety is not uncommon, particularly among performers, and there are studies which confirm their efficacy as anxiolytics. (Schneier 2006)

Since they lower heart rate and reduce tremor, beta blockers have been used by some Olympic marksmen to enhance performance, though beta blockers are banned by the International Olympic Committee (IOC).[2]

Adverse effects

Adverse drug reactions (ADRs) associated with the use of beta blockers include: nausea, diarrhea, bronchospasm, dyspnea, cold extremities, exacerbation of Raynaud's syndrome, bradycardia, hypotension, heart failure, heart block, fatigue, dizziness, abnormal vision, decreased concentration, hallucinations, insomnia, nightmares, depression, sexual dysfunction, erectile dysfunction and/or alteration of glucose and lipid metabolism. Mixed α1/β-antagonist therapy is also commonly associated with orthostatic hypotension. Carvedilol therapy is commonly associated with edema. (Rossi, 2006)

Central nervous system (CNS) adverse effects (hallucinations, insomnia, nightmares, depression) are more common in agents with greater lipid solubility, which are able to cross the blood-brain barrier into the CNS. Similarly, CNS adverse effects are less common in agents with greater aqueous solubility (listed below).

Adverse effects associated with β2-adrenergic receptor antagonist activity (bronchospasm, peripheral vasoconstriction, alteration of glucose and lipid metabolism) are less common with β1-selective (often termed "cardioselective") agents, however receptor selectivity diminishes at higher doses.

A 2007 study (W.J. Elliott, P. Meyer, The Lancet, Jan 20, 2007) revealed that diuretics and beta-blockers used for hypertension increase a patient's risk of developing diabetes. ACE inhibitors and Angiotension Receptor Blockers (ARBs) actually decrease the risk of diabetes. Clinical guidelines in Great Britain, but not in the United States, call for avoiding diuretics and beta-blockers as first-line treatment of hypertension due to the risk of diabetes.

Examples of beta blockers

Dichloroisoprenaline, the first beta blocker.

Non-selective agents

  • Alprenolol
  • Carteolol
  • Levobunolol
  • Mepindolol
  • Metipranolol
  • Nadolol
  • Oxprenolol
  • Penbutolol
  • Pindolol
  • Propranolol
  • Sotalol
  • Timolol

β1-Selective agents

  • Acebutolol
  • Atenolol
  • Betaxolol
  • Bisoprolol
  • Esmolol
  • Metoprolol
  • Nebivolol

Mixed α1/β-adrenergic antagonists

  • Carvedilol
  • Celiprolol
  • Labetalol

β2-Selective agents

  • Butaxamine (weak α-adrenergic agonist activity)

Side Effects / Health Consequences

Comparative information

Pharmacological differences

  • Agents with intrinsic sympathomimetic action (ISA)
    • Acebutolol, carteolol, celiprolol, mepindolol, oxprenolol, pindolol
  • Agents with greater aqueous solubility
    • Atenolol, celiprolol, nadolol, sotalol
  • Agents with membrane stabilising activity
    • Acebutolol, betaxolol, pindolol, propranolol
  • Agents with antioxidant effect
    • Carvedilol

Indication differences

  • Agents specifically indicated for cardiac arrhythmia
    • Esmolol, sotalol
  • Agents specifically indicated for congestive heart failure
    • Bisoprolol, carvedilol, sustained-release metoprolol
  • Agents specifically indicated for glaucoma
    • Betaxolol, carteolol, levobunolol, metipranolol, timolol
  • Agents specifically indicated for myocardial infarction
    • Atenolol, metoprolol, propranolol
  • Agents specifically indicated for migraine prophylaxis
    • Timolol, propranolol

Propranolol is the only agent indicated for control of tremor, portal hypertension and esophageal variceal bleeding, and used in conjunction with α-blocker therapy in phaeochromocytoma (Rossi, 2006).

See also


  • Hjalmarson A, Goldstein S, Fagerberg B, et al. Effects of controlled-release metoprolol on total mortality, hospitalizations, and well-being in patients with heart failure: the Metoprolol CR/XL Randomized Intervention Trial in congestive heart failure (MERIT-HF). MERIT-HF Study Group. JAMA. 2000;283(10):1295-302. PMID 10714728
  • Leizorovicz A, Lechat P, Cucherat M, Bugnard F. Bisoprolol for the treatment of chronic heart failure: a meta-analysis on individual data of two placebo-controlled studies – CIBIS and CIBIS II. Cardiac Insufficiency Bisoprolol Study. Am Heart J. 2002;143(2):301-7. PMID 11835035
  • Packer M, Fowler MB, Roecker EB, et al. Effect of carvedilol on the morbidity of patients with severe chronic heart failure: results of the carvedilol prospective randomized cumulative survival (COPERNICUS) study. Circulation. 2002;106(17):2194-9. PMID 12390947
  • Rossi S, editor. Australian Medicines Handbook 2006. Adelaide: Australian Medicines Handbook; 2006.
  • Stoschitzky K, Sakotnik A, Lercher P, Zweiker R, Maier R, Liebmann P, Lindner W. Influence of beta-blockers on melatonin release. Eur J Clin Pharmacol. 1999 Apr;55(2):111-5. PMID 10335905
  • Schneier FR. Clinical practice. Social anxiety disorder. N Engl J Med. 2006 Sep 7;355(10):1029-36. PMID 16957148.
  • Katzung BG. Basic and Clinical Pharmacology. 9th edition. Lange Medical Books/McGraw-Hill Medical Publishing Division. New York, New York, 2004. Page 130, table 9-3. ISBN: 0-07-144097-6


  1. Sheetal Ladva. NICE and BHS launch updated hypertension guideline. National Institute for Health and Clinical Excellence. URL accessed on 2006-09-30.
  2. World Anti-Doping Agency. The World Anti-Doping Code: The 2006 Prohibited List International Standard. World Anti-Doping Agency. URL accessed on 2006-12-13.

External links

Beta blockers edit
β1 antagonists (cardioselective) edit

{Acebutolol} {Atenolol} {Betaxolol} {Bisoprolol} {Esmolol} {Metoprolol} {Nebivolol}

β2 antagonists (generally Anxiolytic) edit


Non-selective β-blockers edit

{Nadolol} {Oxprenolol} {Propranolol} {Pindolol} {Sotalol} {Timolol}

β2 antagonists (non cardioselective with alpha-blocking activity) edit

{Carvedilol} {Labetalol}

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