Beta blocker

Beta blockers (-blockers, beta-adrenergic blocking

agents, beta antagonists, beta-adrenergic antagonists,
beta-adrenoreceptor antagonists, or beta adrenergic
receptor antagonists) are a class of drugs that are particularly used for the management of cardiac arrhythmias, protecting the heart from a second heart attack
(myocardial infarction) after a rst heart attack (secondary prevention),[1] and hypertension.[2]

Angina pectoris[11][12]

Beta blockers block the action of endogenous

catecholamines
epinephrine
(adrenaline)
and
norepinephrine (noradrenaline) -in particular on
adrenergic beta receptors, of the sympathetic nervous
system, which mediates the ght-or-ight response.[3][4]
Some block all activation of -adrenergic receptors and
others are selective.

Essential tremor

Atrial brillation[13]
Cardiac arrhythmia
Congestive heart failure

Glaucoma
Hypertension
Migraine prophylaxis

Three types of beta receptors are known, designated

1 , 2 and 3 receptors.[5] 1 -adrenergic receptors are
located mainly in the heart and in the kidneys.[4] 2 adrenergic receptors are located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle,
and skeletal muscle.[4] 3 -adrenergic receptors are located in fat cells.[6]

Mitral valve prolapse

Myocardial infarction
Phaeochromocytoma, in conjunction with -blocker

Beta receptors are found on cells of the heart muscles,

smooth muscles, airways, arteries, kidneys, and other tissues that are part of the sympathetic nervous system and
lead to stress responses, especially when they are stimulated by epinephrine (adrenaline). Beta blockers interfere with the binding to the receptor of epinephrine and
other stress hormones, and weaken the eects of stress
hormones.

Postural orthostatic tachycardia syndrome

Symptomatic control (tachycardia, tremor) in
anxiety and hyperthyroidism
Theophylline overdose

In 1962, Sir James W. Black [7] found the rst clinically Beta blockers have also been used for:
signicant beta blockerspropranolol and pronethalol; it
revolutionized the medical management of angina pec Acute aortic dissection
toris[8] and is considered by many to be one of the
most important contributions to clinical medicine and
Hypertrophic obstructive cardiomyopathy
pharmacology of the 20th century.[9]
Marfan syndrome (treatment with propranolol slows
progression of aortic dilation and its complications)

In comparison with other antihypertensive drugs, betablockers are less than optimal for the treatment of primary hypertension, with a raised risk of stroke.[10]

Prevention of variceal bleeding in portal hypertension

Medical uses

Possible mitigation of hyperhidrosis

Large dierences exist in the pharmacology of agents

within the class, thus not all beta blockers are used for
all indications listed below.

Social and other anxiety disorders

Controversially, for reduction of perioperative mortality

Indications for beta blockers include:

1

1.1

Congestive heart failure

ADVERSE EFFECTS

Since they promote lower heart rates and reduce tremors,

beta blockers have been used in professional sports where
high accuracy is required, including archery, shooting,
golf[21] and snooker.[21] Beta blockers are banned by
the International Olympic Committee.[22] A recent, highprole transgression took place in the 2008 Summer
Olympics, where 50 metre pistol silver medallist and 10
metre air pistol bronze medallist Kim Jong-su tested positive for propranolol and was stripped of his medals.

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 ecacy at reducing morbidity and
mortality.[14][15][16] Bisoprolol, carvedilol and sustainedrelease metoprolol are specically indicated as adjuncts
to standard ACE inhibitor and diuretic therapy in congestive heart failure.
For similar reasons, beta blockers have also been used by
Beta blockers are known primarily for their reductive ef- stutterers and surgeons.[23]
fect on heart rate, although this is not the only mechanism
of action of importance in congestive heart failure. Beta
blockers, in addition to their sympatholytic B1 activity in 1.3 Surgery
the heart, inuence the reninangiotensin system at the
kidneys. Beta blockers cause a decrease in renin secre- The use of beta blockers around the time of cardiac
[24]
tion, which in turn reduces the heart oxygen demand by surgery decreases the risk of heart dysrhythmias.
Starting
them
around
the
time
of
other
types
of
surgery;
lowering extracellular volume and increasing the oxygen[24]
carrying capacity of blood. Beta blockers sympatholytic however, worsens outcomes.
activities reduce heart rate, thereby increasing the ejection fraction of the heart despite an initial reduction in
2 Adverse eects
ejection fraction.
Trials have shown beta blockers reduce the absolute risk
of death by 4.5% over a 13-month period. In addition to Adverse drug reactions (ADRs) associated with the use of
reducing the risk of mortality, the number of hospital vis- beta blockers include: nausea, diarrhea, bronchospasm,
its and hospitalizations were also reduced in the trials.[17] dyspnea, cold extremities, exacerbation of Raynauds
syndrome, bradycardia, hypotension, heart failure, heart
block, fatigue, dizziness, alopecia (hair loss), abnormal vision, hallucinations, insomnia, nightmares, sexual
1.2 Anxiety
dysfunction, erectile dysfunction and/or alteration of
Ocially, beta blockers are not approved for anxiolytic glucose and lipid metabolism. Mixed 1 /-antagonist
use by the U.S. Food and Drug Administration.[18] How- therapy is also commonly associated with orthostatic hytherapy is commonly associated
ever, many controlled trials in the past 25 years indicate potension. Carvedilol
[25]
with
edema.
Due
to
the high penetration across the
beta blockers are eective in anxiety disorders, though
bloodbrain
barrier,
lipophilic
beta blockers, such as
[19]
the mechanism of action is not known. The physiologpropranolol
and
metoprolol,
are
more likely than other,
ical symptoms of the ght-or-ight response (pounding
less lipophilic, beta blockers to cause sleep disturbances,
heart, cold/clammy hands, increased respiration, sweat[26]
ing, etc.) are signicantly reduced, thus enabling anxious such as insomnia and vivid dreams and nightmares.
individuals to concentrate on the task at hand.
Musicians, public speakers, actors, and professional
dancers have been known to use beta blockers to avoid
performance anxiety, stage fright and tremor during both
auditions and public performances. The application to
stage fright was rst recognized in The Lancet in 1976,
and by 1987, a survey conducted by the International
Conference of Symphony Orchestra Musicians, representing the 51 largest orchestras in the United States,
revealed 27% of its musicians had used beta blockers
and 70% obtained them from friends, not physicians.[20]
Beta blockers are inexpensive, said to be relatively safe
and, on one hand, seem to improve musicians performances on a technical level, while some, like Barry
Green, the author of The Inner Game of Music, and
Don Greene, a former Olympic diving coach who teaches
Juilliard students to overcome their stage fright naturally,
say the performances may be perceived as soulless and
inauthentic.[20]

Adverse eects associated with 2 -adrenergic receptor

antagonist activity (bronchospasm, peripheral vasoconstriction, alteration of glucose and lipid metabolism) are
less common with 1 -selective (often termed cardioselective) agents, however receptor selectivity diminishes
at higher doses. Beta blockade, especially of the beta1 receptor at the macula densa, inhibits renin release,
thus decreasing the release of aldosterone. This causes
hyponatremia and hyperkalemia.
Hypoglycemia can occur with beta blockade because
2-adrenoceptors normally stimulate hepatic glycogen
breakdown (glycogenolysis) and pancreatic release of
glucagon, which work together to increase plasma glucose. Therefore, blocking 2-adrenoceptors lowers
plasma glucose. 1-blockers have fewer metabolic side
eects in diabetic patients; however, the tachycardia that
serves as a warning sign for insulin-induced hypoglycemia
may be masked. Therefore, beta blockers are to be used
cautiously in diabetics.[27]

3
A 2007 study revealed diuretics and beta blockers used
for hypertension increase a patients risk of developing
diabetes, while ACE inhibitors and angiotensin II receptor antagonists (angiotensin receptor blockers) actually
decrease the risk of diabetes.[28] Clinical guidelines in
Great Britain, but not in the United States, call for avoiding diuretics and beta blockers as rst-line treatment of
hypertension due to the risk of diabetes.[29]
Beta blockers must not be used in the treatment
of cocaine, amphetamine, or other alpha-adrenergic
stimulant overdose. The blockade of only beta receptors increases hypertension, reduces coronary blood
ow, left ventricular function, and cardiac output
and tissue perfusion by means of leaving the alphaadrenergic system stimulation unopposed.[30] The appropriate antihypertensive drugs to administer during
hypertensive crisis resulting from stimulant abuse are
vasodilators such as nitroglycerin, diuretics such as
furosemide and alpha blockers such as phentolamine.[31]

2.1

Contraindications

Patients experiencing bronchospasm due to the 2

receptor-blocking eects of non-selective beta blockers may be treated with anticholinergic drugs, such as
ipratropium, which are safer than beta agonists in patients with cardiovascular disease. Other antidotes for
beta-blocker poisoning are salbutamol and isoprenaline.

3 -Receptor antagonism
Stimulation of 1 receptors by epinephrine and
norepinephrine induces a positive chronotropic and
inotropic eect on the heart and increases cardiac
conduction velocity and automaticity.[37] Stimulation
of 1 receptors on the kidney causes renin release.[38]
Stimulation of 2 receptors induces smooth muscle
relaxation,[39] induces tremor in skeletal muscle,[40] and
increases glycogenolysis in the liver and skeletal muscle.[41] Stimulation of 3 receptors induces lipolysis.[42]

Beta blockers inhibit these normal epinephrine and

norepinephrine-mediated sympathetic actions,[3] but
have minimal eect on resting subjects. That is, they reduce excitement/physical exertion on heart rate and force
of contraction,[43] and also tremor[44] and breakdown of
Beta blockers should not be used as a rst-line treatment glycogen, but increase dilation of blood vessels[45] and
in the acute setting for cocaine-induced acute coronary constriction of bronchi.[46]
syndrome (CIACS). No recent studies have been idenblockers are expected to
tied that show the benet of beta blockers in reducing Therefore, nonselective beta [47]
have
antihypertensive
eects.
The primary antihycoronary vasospasm, or coronary vascular resistance, in
pertensive
mechanism
of
beta
blockers
is unclear, but
patients with CIACS. In the multiple case studies identimay
involve
reduction
in
cardiac
output
(due to negaed, the use of beta blockers in CIACS resulted in detri[48]
tive
chronotropic
and
inotropic
eects).
It may also be
mental outcomes, and the discontinuation of beta blockdue
to
reduction
in
renin
release
from
the
kidneys,
and a
ers used in the acute setting led to improvement in clincentral
nervous
system
eect
to
reduce
sympathetic
activical course. The guidelines by the American College of
Cardiology/American Heart Association also support this ity (for those beta blockers that do cross the bloodbrain
idea, and recommend against the use of beta blockers barrier, e.g. propranolol).
in cocaine-induced ST-segment elevation myocardial in- Antianginal eects result from negative chronotropic and
farction (MI) because of the risk of coronary vasospasm. inotropic eects, which decrease cardiac workload and
Though, in general, beta blockers improve mortality in oxygen demand. Negative chronotropic properties of
patients who have suered MI, it is unclear whether pa- beta blockers allow the lifesaving property of heart rate
tients with CIACS will benet from this mortality reduc- control. Beta blockers are readily titrated to optimal rate
tion because there are no studies assessing use of beta control in many pathologic states.
blockers in the long term, and because cocaine users may
The antiarrhythmic eects of beta blockers arise from
be prone to continue to abuse the substance, thus complisympathetic nervous system blockaderesulting in decating the eect of drug therapy.[32]
pression of sinus node function and atrioventricular
node conduction, and prolonged atrial refractory periods. Sotalol, in particular, has additional antiarrhythmic
2.2 Toxicity
properties and prolongs action potential duration through
[33][34]
Glucagon, used in the treatment of overdose,
in- potassium channel blockade.
Beta blockers are contraindicated in patients with asthma
as stated in the British National Formulary 2011. They
should also be avoided in patients with a history of cocaine use or in cocaine-induced tachycardia.

creases the strength of heart contractions, increases intracellular cAMP, and decreases renal vascular resistance. It is therefore useful in patients with beta-blocker
cardiotoxicity.[35][36] Cardiac pacing is usually reserved
for patients unresponsive to pharmacological therapy.

Blockade of the sympathetic nervous system on renin

release leads to reduced aldosterone via the reninangiotensin-aldosterone system, with a resultant decrease
in blood pressure due to decreased sodium and water retention.

7 EXAMPLES

Intrinsic sympathomimetic activity

Also referred to as intrinsic sympathomimetic eect, this

term is used particularly with beta blockers that can show
both agonism and antagonism at a given beta receptor, depending on the concentration of the agent (beta blocker)
and the concentration of the antagonized agent (usually
an endogenous compound, such as norepinephrine). See
partial agonist for a more general description.
Some beta blockers (e.g. oxprenolol, pindolol, penbutolol
and acebutolol) exhibit intrinsic sympathomimetic activity (ISA). These agents are capable of exerting low
level agonist activity at the -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 after myocardial infarctions, as they have not been demonstrated to be benecial.
They may also be less eective than other beta blockers
in the management of angina and tachyarrhythmia.[25]

Dichloroisoprenaline, the rst beta blocker.

Penbutolol (has intrinsic sympathomimetic activity)

Pindolol (has intrinsic sympathomimetic activity)
Propranolol
Sotalol
Timolol
Eucommia bark (herb) [51]

7.2 1 -selective agents

1 -Receptor antagonism

Some beta blockers (e.g., labetalol and carvedilol) exhibit

mixed antagonism of both - and 1 -adrenergic receptors, which provides additional arteriolar vasodilating action.

Also known as cardioselective

Acebutolol (has intrinsic sympathomimetic activity)
Atenolol
Betaxolol
Bisoprolol

Other eects

Beta blockers decrease nocturnal melatonin release, perhaps partly accounting for sleep disturbances caused by
some agents.[49]
They can also be used to treat glaucoma because they decrease intraocular pressure by lowering aqueous humor
secretion.[50]

Celiprolol
Esmolol[52]
Metoprolol
Nebivolol (also increases nitric oxide release for vasodilation)

7.3 2 -selective agents

Examples

7.1

Nonselective agents

Bucindolol
Carteolol
Carvedilol (has additional -blocking activity)
Labetalol (has additional -blocking activity)
Nadolol
Oxprenolol (has intrinsic sympathomimetic activity)

Butaxamine (weak -adrenergic agonist activity):

No common clinical applications, but used in experiments.
ICI-118,551: Highly selective 2 -adrenergic receptor antagonistno known clinical applications, but
used in experiments due to its strong receptor specicity.

7.4 3 -selective agents

SR 59230A (has additional -blocking activity):
Used in experiments.

Comparative information

8.1

Pharmacological dierences

Agents with intrinsic sympathomimetic action (ISA)

Acebutolol, carteolol, celiprolol, mepindolol,
oxprenolol, pindolol
Agents with greater aqueous solubility (hydrophilic
beta blockers)
Atenolol, celiprolol, nadolol, sotalol
Agents with membrane stabilizing eect

Indication dierences

Agents specically indicated for cardiac arrhythmia

Esmolol, sotalol, landiolol
Agents specically indicated for congestive heart
failure
carvedilol, sustained-release
bisoprolol, nebivolol

metoprolol,

Agents specically indicated for glaucoma

Betaxolol,
carteolol,
metipranolol, timolol

levobunolol,

Agents specically indicated for myocardial infarction

Atenolol, metoprolol, propranolol
Agents specically indicated for migraine prophylaxis
Timolol, propranolol

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8.2

10 References

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[6] Clment K, Vaisse C, Manning BS, Basdevant A,
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Alpha blockers

[12] Khan, M.I. Gabriel (2007). Cardia Drug Therapy. Humana Press. ISBN 1-59745-238-6.

10

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11 External links
Musicians and beta-blockers by Gerald Klickstein,
March 11, 2010 (A blog post that considers
whether beta-blockers are safe, eective, and appropriate for performers to use.)
Better Playing Through Chemistry by Blair Tindall,
New York Times, October 17, 2004. (Discusses the
use of beta blockers among professional musicians)
Musicians using beta blockers by Blair Tindall.
Condensed version of above article.
In Defense of the Beta Blocker by Carl Elliott, The
Atlantic, August 20, 2008. (Discusses the use of
propranolol by a North Korean pistol shooter in the
2008 Olympics)
beta-Adrenergic Blockers at the US National Library of Medicine Medical Subject Headings
(MeSH)

12

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12.1

TEXT AND IMAGE SOURCES, CONTRIBUTORS, AND LICENSES

Text and image sources, contributors, and licenses

Text

Beta blocker Source: http://en.wikipedia.org/wiki/Beta%20blocker?oldid=640247115 Contributors: AxelBoldt, Kpjas, Edward, Patrick,

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and Anonymous: 255

12.2

Images

File:Dichloroisoprenaline.svg Source: http://upload.wikimedia.org/wikipedia/commons/6/6a/Dichloroisoprenaline.svg License: CC

BY-SA 3.0 Contributors: Self-made using BKChem and Inkscape Original artist: JaGa

12.3

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