• Clinical science

Beta blockers (Beta antagonists)


Beta blockers are a group of drugs that inhibit the sympathetic activation of β-adrenergic receptors. Cardioselective blockers (e.g., atenolol, bisoprolol) primarily block β1 receptors in the heart, causing decreased heart rate, cardiac contractility, cardiac workload, and AVN conduction. Nonselective beta blockers (e.g., pindolol, propranolol) inhibit all β receptors and may cause bronchoconstriction, peripheral vasoconstriction, and metabolic imbalances (e.g., hypoglycemia and hyperglycemia, hypertriglyceridemia) in addition to cardiac effects. Cardioselective beta blockers have a lower side-effect profile and are preferred in the management of coronary heart disease, compensated heart failure, acute coronary syndrome, and certain types of arrhythmias. Propranolol, a nonselective beta blocker, is the first-line drug in the management of essential tremor, portal hypertension, migraine prophylaxis, and thyroid storm. Beta blockers are contraindicated in patients with symptomatic bradycardia, AV block, decompensated heart failure, and asthma. Initiation and cessation of beta-blocker therapy should always be gradual to avoid side effects or symptoms of withdrawal (e.g., rebound tachycardia, hypertension, acute cardiac death).


Type Agents Effects Side effects Indications
Cardioselective beta blockers (β1 selective) With ISA
Without ISA
Nonselective beta blockers1, β2, and β3 receptors) With ISA
  • Block β1, β2, and β3 receptors
  • Sotalol also blocks cardiac potassium channels (antiarrhythmic effect).
Without ISA
With additional α-blocking action

With the exception of nebivolol, all cardioselective beta blockers begin with the letters A to M (B1 = first half of the alphabet). Except for beta blockers with alpha-blocking action, all noncardioselective beta blockers begin with the letters N to Z (B2 = second half of the alphabet).



Beta blockers competitively bind to and block β-adrenergic receptors, thereby inhibiting sympathetic (adrenergic and/or noradrenergic) stimulation of β receptors. See the sympathetic vs. parasympathetic nervous system for details regarding the effects of β-adrenergic stimulation.

Effects of β-adrenergic blockade

Types of β receptors Main site of action Effects of β-adrenergic blockade
β1 Heart
  • Anti-ischemic effect: β1 blockadeheart rate and ↓ cardiac contractility↓ BP and ↓ oxygen consumption by the heartanti-ischemic effect
  • Antiarrhythmic effect: β1 blockade AVN conduction, AVN refractory time, and heart rate → anti-arrhythmic effect
  • Anti-remodeling effect
  • β1 blockade of the juxtaglomerular cellsrenin release → angiotensin II conversion → ↓ H2O resorption↓ BP
β2 Smooth muscle
  • Vasculature: vasoconstriction
  • Bronchioles: bronchoconstriction
Ciliary body of the eye
Pancreatic beta cells
Skeletal muscle
  • ↓ Glucose uptake (insulin sensitivity)
Lipoprotein lipase enzyme
β3 Adipose tissue

Beta blockers competitively inhibit adrenergic substances (e.g., adrenaline, noradrenaline) at β receptors!
A rule to remember the main effector organs for β receptors: There is 1 heart - β1 blockers act on the heart; there are 2 lungs - β2 blockers affect bronchial smooth muscles.

Intrinsic sympathomimetic activity (ISA) [7]


Adverse effects


Beta blocker adverse effects

Nonselective beta blockers and cardioselective beta blockers

(β1-receptor and β2-receptor blockade)



Cholesterol levels

Nonselective beta blockers

(β2-receptor blockade)

Peripheral vasculature

Beta blockers should be introduced gradually with slow increases in dosage and slowly tapered off when no longer needed.

Beta-blocker withdrawal

Beta-blocker overdose


We list the most important adverse effects. The selection is not exhaustive.


Cardiovascular indications

Specific indications for propranolol




Absolute contraindications Relative contraindications


We list the most important contraindications. The selection is not exhaustive.

last updated 08/31/2020
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