Beta blockers (sometimes written as β-blocker) is a class of drugs used for various indications, but particularly for the management of cardiac arrhythmias, cardioprotection after myocardial infarction (heart attack), and hypertension.
As beta adrenergic receptor antagonists, they diminish the effects of epinephrine (adrenaline) and other stress hormones. Invented by Sir James W. Black in the late 1950s, Propranolol was the first clinically useful beta blocker; it revolutionized the medical management of angina pectoris and is considered to be one of the most important contributions to clinical medicine and pharmacology of the 20th century.
Beta blockers may also be referred to as beta-adrenergic blocking agents, beta-adrenergic antagonists, or beta antagonists.
Examples of beta-blockers include: acebutolol, betaxolol,
bisoprolol, esmolol, propranolol, atenolol, labetalol, carvedilol,
metoprolol, and nebivolol.
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, 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 expected that non-selective beta blockers
have an antihypertensive effect. 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 (for those
β-blockers that do cross the blood-brain barrier, e.g. Propranolol).
Antianginal effects result from negative chronotropic and
inotropic effects, which decrease cardiac workload and oxygen demand.
Negative chronotropic properties of beta blockers allow the lifesaving
property of heart rate control. Beta blockers are readily titrated to
optimal rate control in many pathologic states.
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 water retention.
Intrinsic sympathomimetic activity
Also referred to as intrinsic sympathomimetic effect, 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
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 in 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.
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.
Beta blockers protect against social anxiety: "Improvement
of physical symptoms has been demonstrated with beta-blockers such as
propranolol; however, these effects are limited to the social anxiety
experienced in performance situations." (example: an inexperienced
symphony soloist)
Beta blockers can impair the relaxation of bronchial muscle
(mediated by beta-2) and so should be avoided by asthmatics.
They can also be used to treat glaucoma because they
decrease intraocular pressure by lowering aqueous humor secretion.
Further Reading
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